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Isoquercitrin is a natural flavonoid quercetin with anti-inflammatory, anti-anaphylactic, antiviral, and anticancer activities. Here, we investigated the effect of isoquercitrin on immunogenic cell death (ICD) of gastric cancer (GC). The effect of isoquercitrin on GC cell lines (AGS and HGC-27) was evaluated using cell counting kit-8 assays, colony formation assays, Annexin V/PI apoptosis detection kit, western blot analysis, JC-1 staining, immunofluorescence assays, and enzyme-linked immunosorbent assay. Isoquercitrin at doses greater than 20 μM had significant inhibitory effects on the survival of GC cell lines, including HGC-27, AGS, MKN-45, and SNU-1. Isoquercitrin treatment decreased GC cell colony formation in a dose-dependent manner and induced apoptosis accompanied by downregulation of BCL-2 and upregulation of BAX, cleaved caspase-3, and caspase-12. In addition, isoquercitrin promoted the disruption of mitochondrial membrane potential in GC cells. The GC cell surface levels of calreticulin (CRT) and extracellular levels of CRT, ATP, and HMGB1 were enhanced by treatment with isoquercitrin. The protein levels of HMGB1, HSP70, and HSP90 were upregulated by isoquercitrin in a dose-dependent manner. Moreover, the endoplasmic reticulum (ER) stress inhibitor 4-phenylbutyrate reversed isoquercitrin-induced ICD in GC cells. Overall, our data suggested that isoquercitrin induces ER stress and ICD in GC cells. Isoquercitrin may be a candidate anticancer drug for the treatment of GC.

This study aimed to investigate the effects of luteolin on colorectal cancer (CRC) and explore its underlying mechanism. HCT-116 and HT-29 cells were treated with luteolin, cisplatin, or selumetinib. The cell survival, cell proliferation, apoptosis and cell cycle distribution, and DNA damage were detected using Cell Counting Kit-8, colony formation, flow cytometry, and immunofluorescence staining analysis, respectively. Western blotting was used to detect the expression of apoptosis-related, cycle-related, DNA-damage-related, and mitogen-activated protein kinase (MAPK) pathway-related proteins. Luteolin showed inhibitory effects on cellular growth by reducing cell survival and proliferation, inducing apoptosis and DNA damage, and arresting the cell cycle in a concentration-dependent manner in HCT-116 and HT-29 cells. Meanwhile, luteolin increased the expression of pro-apoptotic proteins, p-CHK1 (central to the induction of cell cycle arrest), and DNA excision repair protein and decreased anti-apoptotic proteins, G2-M phase-related proteins, and DNA repair proteins. The combination of cisplatin and luteolin significantly decreased cell survival and increased the apoptosis rate of HCT-116 and HT-29 cells compared with cisplatin alone. Bioinformatic analysis using the Comparative Toxicogenomics Database and STITCH and MalaCards databases showed that the MAPK pathway is involved in the pharmacology of luteolin. Furthermore, western blotting demonstrated that luteolin plays an inhibitory role by suppressing the MAPK signaling pathway in CRC, which is enhanced when combined with selumetinib. Luteolin can also prevent tumourigenesis in CRC in vivo. In conclusion, luteolin suppressed cell proliferation, blocked the cell cycle, and induced DNA damage and apoptosis progression in CRC cells by mediating the MAPK pathway.

Background. Gliomas are the most common and most malignant primary tumors of the adult central nervous system, but their etiology and pathogenesis remain unclear. This study was aimed at investigating the expression and function of lncRNA PDCD4-AS1 in glioma and elucidating the mechanism by which PDCD4-AS1 regulates the biological features of glioma. Method. The expression of PDCD4-AS1 was determined by bioinformatic analysis and qRT-PCR assay. PDCD4-AS1 was knocked down in glioma cells using siRNA transfection. The functional analysis of cells was conducted using CCK-8 proliferation, cell migration, and invasion assays, as well as cell cycle analysis. An in vivo tumorigenesis assay was performed to investigate the role of PDCD4-AS1 knockdown in glioma tumor growth. We performed bioinformatic analysis, RNA pull-down, and luciferase reporter assays to investigate the downstream targets of PDCD4-AS1. A rescue experiment was then performed to confirm the regulating mechanism. Results. PDCD4-AS1 was found to be significantly upregulated in glioma patients’ tumor tissues and cell lines. The silencing of PDCD4-AS1 inhibited glioma cell proliferation, invasion, migration, and induced cell cycle arrest. In vivo experiments showed that silencing PDCD4-AS1 inhibited glioma tumor growth. An investigation of the underlying mechanism suggested that PDCD4-AS1 positively regulated METTL7B expression by sponging miR-30b-3. Both the knockdown of miR-30b-3p and the overexpression of METTL7B could, respectively, reverse the malignant phenotype of cells affected by silencing PDCD4-AS1. Conclusion. These results demonstrate that PDCD4-AS1 exerted an oncogenic role by regulating the miR-30b-3p/METTL7B axis.

Tripartite motif-containing protein 11 (TRIM11) and family with sequence similarity 46B (FAM46B) have been demonstrated to play roles in prostate cancer development, but their function in paclitaxel resistance remains unclear. The role of TRIM11 and FAM46B in paclitaxel resistance in prostate cancer was estimated. The paclitaxel-resistant cells were established with gradually increasing concentrations of paclitaxel in prostate cancer cells. The sensitivity to paclitaxel of established cells was assessed by the value of the median inhibitory concentration in the presence of 0-1000 nM paclitaxel. The expression level of TRIM11 and FAM46B was evaluated by real-time quantitative polymerase chain reaction. The proliferation, migration, and invasion of established cells were evaluated by CCK8 and Tran-swell assay. TRIM11 was upregulated in paclitaxel-resistant cells and promoted the proliferation, migration, and invasion of established cells. The significant downregulation of FAM46B was observed in paclitaxel-resistant cells. Although the overexpression of FAM46B suppressed the viability and metastasis of paclitaxel-resistant cells, which was reversed by the upregulation of TRIM11. Both the knockdown of TRIM11 and overexpression of FAM46B could enhance paclitaxel sensitivity of established resistant cells. The promoted effect of FAM46B overexpression was alleviated by the elevation of TRIM11. TRIM11 could improve the sensitivity to paclitaxel of resistant prostate cancer cells via regulating FAM46B.

The present study was undertaken to decipher the role of HOXC10 gene in regulating the growth and metastasis of prostate cancer. The results revealed significant (p

Background: Renal cell carcinoma (RCC) is a common malignant tumor of the urinary system with a high recurrence rate and easy metastasis. Current clinical drugs for renal cell carcinoma include immunotherapies and targeted drugs. Axitinib is a clinically targeted drug for treating renal cell carcinoma, which has shortcomings such as unstable efficacy and easy drug resistance. Therefore, this study aimed to determine whether embelin can enhance the sensitivity of renal cancer cells to axitinib and explore its regulatory pathways. Methods: The enhancing effect of embelin on axitinib was detected using MTT, crystal violet staining and annexin V-FITC staining in two renal cancer cell lines. Western blot was performed to detect the expression of autophagy-related proteins under different conditions. Bioinformatic tools were used to predict the pathways through which embelin may act on renal cancer cells, and pharmacological methods were used to verify the results. Results: Embelin enhanced the sensitivity of renal cancer cells to axitinib in the following aspects: enhancing the inhibition of cell proliferation by axitinib, and the induction of cell apoptosis. HIF was a potential pathway for Embelin action. After IOX2 regulated the HIF-1α pathway, the enhancing effect of embelin on axitinib was weakened. Moreover, after PT2977 regulated the HIF-2α pathway, the enhancing effect of embelin on axitinib was weakened. Conclusions: Embelin enhanced the sensitivity of A498 and 786-O renal cancer cells to axitinib by inhibiting the HIF pathway.

Objective Increased dependence on glycolysis is a known element of cancer. This study was designed to examine critical glycolysis components including transcription factor MYC and its downstream target lactate dehydrogenase A (LDHA), potential upstream regulators of glycolysis such as family with sequence similarity 46 member B (FAM46B), and the impact of the abundance of these proteins on apoptosis and glycolysis in prostate cancer. Materials and methods A total of 70 primary prostate cancer patient samples were compared to normal tissues for FAM46B and LDHA expression and the corresponding patients' survival was monitored for 60 months. Prostate cancer cell lines were employed for protein expression manipulation, glucose uptake and LDH assays, and apoptosis measurements. A xenograft mouse model was used to quantify the role of FAM46B and LDHA on tumor growth in vivo. Results FAM46B expression was reduced in prostate tumor tissue compared to normal tissue and prostate cancer patients who expressed low amounts of FAM46B had shortened average lifespans compared to those who expressed higher amounts of FAM46B (p=0.008). FAM46B overexpression reduced glucose uptake, decreased LDH activity, and induced apoptosis in prostate cancer cell lines while FAM46B shRNA increased MYC levels in a non-malignant prostate cell line (P69). Conversely, forced expression of LDHA in LNCaP cells produced an increase in glycolysis markers with a corresponding decrease in apoptosis. FAM46B-overexpressing xenografts had starkly blunted growth which was restored with co-overexpression of LDHA. Conclusion FAM46B plays a central role in regulating glycolysis and apoptosis in prostate cancer and operates through the regulation of LDHA via MYC. FAM46B's keystone status in prostate cancer makes it a potential, robust biomarker for prostate cancer prognosis and a promising therapeutic target.

This study aimed to determine the apoptosis and autophagy-inducing mechanism of atractylodin in human breast cancer MCF-7 cells. The molecular mechanism of anticancer activity of atractylodin was confirmed by assessing the levels of reactive oxygen species (ROS) level, lipid peroxidation (LPO), antioxidants activity, dual staining, and comet assay. Moreover, cleaved caspases 3, 8, and 9, and signaling proteins, such as p53, Bcl-2, and Bax, phosphatidylinositol-3-kinase/protein kinase B/mammalian target of rapamycin(P13K/Akt/mTOR), LC3I and LC3II, and beclin-1 were analyzed. In MCF-7 cells treated with atractylodin, the concentration-dependent toxicity, increased LPO, increased production of ROS, and decreased activity of superoxide dismutase, catalase, and glutathione peroxidasewere observed. In MCF-7 cells, atractylodin administration decreased Bcl-2 expression while activating the expression of p53, Bax, cleaved caspase-3, caspase-8, and caspase-9 apoptotic members. Furthermore, atractylodin blocked the P13K/Akt/mTOR signaling pathway, increased the conversion of LC3I to its lipidated form of LC3II, and increased beclin-1 expression, whereas downregulated the p62 expression in MCF-7 cells. As a result, altering apoptotic and autophagy-related biomarkers, atractylodin triggered apoptosis and autophagy in MCF-7 cells. As a result, atractylodin could be utilized to treat human breast cancer after the proper clinical trial.

To investigate the effect of long noncoding RNA ST8SIA6-AS1 on the epithelial-to-mesenchymal transition (EMT) and angiogenesis of pituitary adenoma and its possible mechanism. The expression levels of ST8SIA6-AS1 and HOXA9 in noninvasive pituitary adenoma and invasive pituitary adenoma were detected using qRT-PCR. sh-ST8SIA6-AS1 transfection silenced the expression of ST8SIA6-AS1 in GH3 and GTI-1 cells. The effects of ST8SIA6-AS1 on the proliferation, invasion, angiogenesis, and EMT of GH3 and GTI-1 pituitary adenoma cells were detected. The migration ability of cells was detected through scratch assay. Dual luciferase analysis verified the targeting relationship between ST8SIA6-AS1 and miR-5195-3p. ST8SIA6-AS1 and HOXA9 were highly expressed in invasive pituitary adenoma. In pituitary adenomas, miR-5195-3p directly targeted HOXA9. miR-5195-3p is the target gene of ST8SIA6-AS1. ST8SIA6-AS1 knockdown inhibited the proliferation, invasion, angiogenesis, and EMT of pituitary adenoma. HOXA9 expression mediates the biological effect of ST8SIA6-AS1. ST8SIA6-AS1 targets miR-5195-3p to regulate the expression of HOXA9 and promote the EMT of pituitary adenomas.

This study is aimed at investigating the effect and mechanism of long noncoding RNA (lncRNA) KCNQ1OT1 on pituitary adenoma (PA). The KCNQ1OT1 expression in invasive and noninvasive PA tissues was detected by real-time fluorescence quantitative polymerase chain reaction (qPCR). The effects of KCNQ1OT1 on the proliferation of PA cells, namely, GH3 and HP75, were detected by CCK-8 experiment. The Transwell assay detected the effect of KCNQ1OT1 on the invasion of GH3 and HP75 cells. The effect of KCNQ1OT1 on the clonal formation ability was detected by clonal formation experiment. The double luciferase reporter assay and the miRNA pull down assay verified the binding of KCNQ1OT1 to miR-140-5p. Meanwhile, the regulatory effect of miR-140-5p on RAB11A was verified. qPCR results showed that KCNQ1OT1 was significantly increased in invasive PA compared with noninvasive PA tissues. Knockdown KCNQ1OT1 inhibited PA cell stemness, angiogenesis, and EMT. In addition, knockdown KCNQ1OT1 inhibited the proliferation, invasion, and clonal formation of PA. miR-140-5p is the target gene of KCNQ1OT1. miR-140-5p targets RAB11A directly. RAB11A can mediate the biological effects of KCNQ1OT1. Meanwhile, lncRNA KCNQ1OT1 can promote the EMT and cellular stemness of PA. Its mechanism of action is realized by inhibiting miR-140-5p. This result can provide a molecular basis for the further study of PA.

Background Renal cell carcinoma (RCC) is a common malignant tumor of urinary system with high recurrence rate and easy metastasis. Current clinical drugs for renal cell carcinoma include immunotherapy and targeted drugs. Axitinib is a clinical targeted drug for the treatment of renal cell carcinoma, which has some shortcomings such as unstable efficacy and easy drug resistance. The aim of this study was to determine whether embelin can enhance the sensitivity of renal cancer cells to axitinib and explore its regulatory pathways. Results Embelin enhanced the sensitivity of renal cancer cells to axitinib in the following aspects: enhancing the inhibition of cell proliferation by axitinib, the ability to kill cancer cells, and the induction of cell apoptosis. HIF-1α was a potential pathway of Embelin action. After IOX2 regulated the HIF-1α pathway, the enhancing effect of embelin on axitinib was weakened. Conclusions Embelin enhanced the sensitivity of both A498 and 786-O renal cancer cells to axitinib by inhibiting the HIF-1α pathway.

Raman spectra of β-carotene aggregates are measured in ethanol-water solution at different temperatures. The aim is to study in detail the Raman spectra of these aggregates in ethanol/water solution at room temperature and their changes with temperature. When the temperature is reduced from 295 K to 77 K, the Raman band is almost unchanged. The CC stretching mode of the β-carotene aggregate shows a relatively small frequency shift compared to the organic solvent due to the frequency shift and the change of the resonance condition. By fitting the experimental results, it was shown that the prominent peak at 1522 cm−1 can be deconvoluted into two closely spaced modes. The frequency shifts of these two modes show similar trends, and their resonance enhancements are different. The 0-0 and 0–1 bands of the β-carotene aggregates behave differently before and after the solution phase transition by background extraction when lowering the temperature. The solution phase transition also leads to a dramatic fluorescence quenching of the β-carotene aggregates. In the solid state, the fluorescence enhancement of the 0–1 band can be found, while the 0-0 band shows a decreasing trend. The results showed that the β-carotene aggregates retained weakly coupled aggregates at 77 K while exhibiting H-like temperature dependence in ethanol/water solution.

Raman spectra of acetonitrile-water mixtures are measured in different acetonitrile concentration fractions. The nitrile stretch (v2) and the combination (v3 + v4) modes are coupled by Fermi resonance. We extract the Fermi resonance parameters and find that the frequency separation shows non-linear dependence as a function of acetonitrile concentration fractions. v2 ~ v3 + v4 Fermi doublets intensity ratio exhibits nonlinearity, which is accelerated with the decreasing of the Fermi coupling strength. The OH stretching region is also investigated in order to reveal the variation of the water structure. Our data show that there are strong relationships between the intensity of ~3225 cm−1 band and the v2~v3 + v4 Fermi resonance. Because the nitrile stretch and Fermi resonance are very environmental sensitive, the nonlinear modulation on Fermi resonance and the non-regular intensity ratio are attributed to the change of water hydrogen-bonding network. The results provide useful structural and spectral insights for the design of new experiments and the molecular structure modeling.

Background and objectives Osteoarthritis (OA) is a widespread degenerative joint disease characterized by articular cartilage degradation and is the leading cause of physical disability. Noncoding RNAs, especially long noncoding RNAs (lncRNAs) and microRNAs, are involved in the degradation of the chondrocyte extracellular matrix (ECM) in patients with OA. The present study was aimed to investigate the effects of lncRNA and miR-22 on the degradation of the chondrocyte ECM and underlying mechanisms. Methods To simulate conditions found in OA, primary cultured chondrocytes were treated with IL-1, TGF-β, or sb525334. Real-time PCR and Western blot analysis were performed to detect expressions of miR-22, lncRNA-TM1P3, ALK1, MMP13, pSMAD1/5, SMAD1, and pSMAD5. Small interfering RNAs and a miR-22 mimic or inhibitor were utilized to determine lncRNA-TM1P3 knockdown and miR-22 overexpression or inhibition. Results The lncRNA-TM1P3 significantly upregulated in patients with OA, accompanied by the downregulation of miR-22 and upregulation of pSMAD1/5 and MMP13, which ultimately resulted in the degradation of the chondrocyte ECM in patients with OA. Bioinformatics analysis predicted miR-22 as a target of both lncRNA-TM1P3 and MMP13. The lncRNA-TM1P3 knockdown significantly increased the expression of ALK1, a corresponding increase in ECM degradation was observed by affecting the phosphorylation of SMAD1/5 and the expression of MMP13, which did not affect the expression of ALK1. Conclusions These findings demonstrated that the lncRNA-TM1P3/miR-22/TGF-β signaling/MMP13 axis is involved in the degradation of chondrocyte ECM in patients with OA, which could provide novel therapies for OA treatment.

FAM46B is a member of the family with sequence similarity 46. Little is known about the expression and functional role(s) of FAM46B in prostate cancer (PC). In this study, the expression of FAM46B expression in The Cancer Genome Atlas, GSE55945, and an independent hospital database was measured by bioinformatics and real-time PCR analysis. After PC cells were transfected with siRNA or a recombinant vector in the absence or presence of a β-catenin signaling inhibitor (XAV-939), the expression levels of FAM46B, C-myc, Cyclin D1, and β-catenin were measured by western blot and real-time PCR. Cell cycle progression and cell proliferation were measured by flow cytometry and the CCK-8 assay. The effects of FAM46B on tumor growth and protein expression in nude mice with PC tumor xenografts were also measured. Our results showed that FAM46B was downregulated but that β-catenin was upregulated in patients with PC. FAM46B silencing promoted cell proliferation and cell cycle progression in PC, which were abrogated by XAV-939. Moreover, FAM46B overexpression inhibited PC cell cycle progression and cell proliferation in vitro and tumor growth in vivo. FAM46B silencing promoted β-catenin protein expression through the inhibition of β-catenin ubiquitination. Our data clearly show that FAM46B inhibits cell proliferation and cell cycle progression in PC through ubiquitination of β-catenin., Prostate cancer: getting earlier diagnosis A little-studied protein may help in early diagnosis and treatment of prostate cancer (PC), one of the most common cancers in men. Because early-stage PC causes few symptoms, many patients are not diagnosed until later stages, when treatment options are limited. New methods for early diagnosis and treatment are actively sought. Proteins in the FAM46 family are known to be involved in many types of cancer. Dongliang Yan at Shanghai Sixth People’s Hospital East and co-workers investigated what role one protein in this family, FAM46B, might play in PC. Analysis of tumor samples showed that FAM46B levels were much lower in PC than in healthy tissues. These changes were linked to another tumor-associated protein, β-catenin. In further tests in mice, artificially increasing FAM46B levels decreased tumor size. These results could improve treatments for PC.

Background. Neurovascular-related genes have been implicated in the development of cancer. Studies have shown that a high expression of neuropilins (NRPs) promotes tumourigenesis and tumour malignancy. Method. A multidimensional bioinformatics analysis was performed to examine the relationship between NRP genes and prognostic and pathological features, tumour mutational burden (TMB), microsatellite instability (MSI), and immunological features based on public databases and find the potential prognostic value of NRPs in pancancer. Results. Survival analysis revealed that a low NRP1 expression in adrenocortical carcinoma (ACC), cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), low-grade glioma (LGG), and stomach adenocarcinoma (STAD) was associated with poor prognosis. A high NRP2 expression in bladder urothelial carcinoma (BLCA), kidney renal papillary cell carcinoma (KIRP), and mesothelioma (MESO) was associated with poor prognosis. Moreover, NRP1 and NRP2 were associated with TMB and MSI. Subsequent analyses showed that NRP1 and NRP2 were correlated with immune infiltration and immune checkpoints. Genome-wide association analysis revealed that the NRP1 expression was strongly associated with kidney renal clear cell carcinoma (KIRC), whereas the NRP2 expression was closely associated with BLCA. Ultimately, NRP2 was found to be involved in the development of BLCA. Conclusions. Neurovascular-related NRP family genes are significantly correlated with cancer prognosis, TME, and immune infiltration, particularly in BLCA.

Phase transition occurring during cycling plays a fundamentally important role in the cycling performance of nickel-rich cathodes. Here, splitting of two O3 phases, rather than the often observed O1 phases in the conventional LiCoO$_{2}$ electrode, was discovered in LiNi$_{0.85}$Co$_{0.10}$Mn$_{0.05}$O$_{2}$ at a high-voltage region (>4.6 V). Such degradation could be mitigated via Al doping.

Plant bio constituents have the ability to prepare nanoparticles, and usually, plant polyphenols are tested to reduce sodium selenite to selenium nanoparticles (SeNPs). In this work, we showed the biosynthesis of SeNPs using Ocimum tenuiflorum leaf extract. The as obtained SeNPs were in the size range of 15–20 nm and spherical in shape. Also, TEM microscopic images represented the aggregation of crystal structures as extracellular deposits. Moreover, scanning electron microscopy was performed to examine the chemical transition of calcium oxalate (CaC(2)O(4)) crystal’s shape and structure due to the influence of SeNPs. SeNPs inhibited the aggregation and growth of CaC(2)O(4) monohydrate crystals and hence the prepared SeNPs could have important prospects in medical and pharmaceutical applications as a potential inhibitor of CaC(2)O(4) urinary stones.

The aim of the present study was to determine whether it was possible to repair urethral defects with a material of adipose mesenchymal stem cells (ADMSCs)‑porous silk fibroin (SF). A total of 39 male New Zealand white rabbits were randomly divided into a control group, an SF group and a bromodeoxyuridine (BrdU)‑labeled ADMSCs‑SF group (SSF group; n=13/group). Defects were made by resecting the posterior urethral wall. The defects in the SF and SSF groups were repaired using SF and BrdU‑labeled ADMSCs‑SF materials respectively. Then the anterior wall was sutured, and the urethral catheter was retained for 3 weeks following surgery. The catheter was rinsed with nitrofurazone once a day. The cells with positive expressions of factor VIII related antigen (FVIII‑RAg), α‑smooth muscle actin (α‑SMA) and pan‑cytokeratin (AE1/AE3) were detected by immunohistochemical assay, and the distributions of BrdU positive cells and macrophages were observed. Urethrography was performed prior to and following surgery. All rabbits had normal urethral morphologies prior to surgery. The incidence rates of postoperative complications in the control, SF and SSF groups were 76.92 (7/13), 23.07 (3/13) and 15.38% (2/13), respectively (P

Absorption, resonance Raman spectra are reported on all-trans-β-carotene dissolved in different polarizability solvents. The absorption spectra of all-trans-β-carotene are analyzed by Franck-Condon principle and the Huang-Rhys factors are calculated. With the increasing solvent polarizability, the Huang-Rhys factor and the electron-phonon coupling constant decrease, while the Raman scattering cross section increases. The red-shift of absorption would leads to an increasing spectral overlap with the laser excitation leading to an enhanced resonance effect. Through electron-phonon coupling, the ground state structure of all-trans-β-carotene will be modulated by the electronic transition and is assumed to lead to a modulation of energy flow. Results present insights on the solvent's polarizability dependence on electron-phonon coupling of carotenoid. This work is expected to be helpful for exploring the surrounding medium effects on the electronic transition and carbon‑carbon vibrations.

BACKGROUND To explore the time-dependent effects of acupuncture on mRNA levels of the apoptotic factors BCL-2 and BAX in a rat cerebral hemorrhage model, slow injection of autologous blood to the caudate nucleus was used to generate the cerebral hemorrhage model. MATERIAL AND METHODS A sham surgery control group, groups with acupuncture applied 3, 9, 24, and 48 hours after model induction, and time-matched model-only control groups were used. In situ hybridization was used to detect BCL-2 and BAX mRNA expression, and semi-quantitative RT-PCR was used to measure the expression. RESULTS The number of BCL-2 and BAX mRNA-positive cells significantly increased during the acute phase of cerebral hemorrhage. BCL-2 mRNA was significantly upregulated in acupuncture groups compared to other groups, whereas BAX mRNA levels in the acupuncture groups were lower in the other groups, except for the sham surgery group. Additionally, earlier acupuncture intervention was associated with a lower ratio of expression between the two genes. Changes in BCL-2 and BAX mRNA expression were consistent with changes in the number of cells positive for BCL-2 and BAX mRNA; however, the change in the expression ratio was consistent with the change in the number of cells positive for BCL-2 mRNA, but opposite to the change in the number of cells positive for BAX mRNA. CONCLUSIONS Acupuncture ameliorated changes in expression of apoptotic factors in the brain induced by acute cerebral hemorrhage and may thus protect the brain, with greater efficacy when the delay before acupuncture was minimized.

Raman scattering from liquid carbon disulfide has been studied for different concentrations in benzene. Modes ν 1 (656 cm −1 ) and 2ν 2 (796 cm −1 ) are allowed bands of carbon disulfide, while ν 2 (396 cm −1 ) is forbidden by the selection rules. However, a weak band has been observed along with the strong allowed totally symmetrical stretching mode ν 1 . The observation is ascribed to the effects of the vibrational anharmonicity of free molecule and intermolecular interaction potential. The ν 1 and 2ν 2 Fermi resonance can be influenced by the external conditions. The effects of the ν 1 and 2ν 2 Fermi resonance on the Raman frequency and relative intensity are discussed and the Raman scattering cross section of ν 2 is studied for different concentration of carbon disulfide in benzene. The second-order perturbation quantum theory is introduced to explain the results that the Raman scattering of ν 2 is influenced by 2ν 2 and its Fermi resonance with ν 1 .

Background Renal cancer represents about 3 % of all human cancers. Clear cell renal cell carcinoma (ccRCC) is the main type of renal cancer. Methionine sulfoxide reductase B3 (MSRB3) is a protein repair enzyme that specifically catalyzes the reduction of methionine-R-sulfoxide residues and has an antioxidant function. However, MSRB3’s role in ccRCC is still obscure. Methods Immunohistochemical staining and Real-time PCR were used to compare the expression level of MSRB3 in ccRCC tissues and adjacent tissues. Western blot was used to detect the expression of MSRB3 in cell lines. Chi-square test were applied to evaluate the potential of MSRB3 to function as a cancer biomarker. RNA interference was used to inhibit MSRB3 expression in ccRCC cells, followed by detecting cell proliferation, apoptosis, migration and invasion. The markers of endoplasmic reticulum stress were then detected by western blot. Results In this study, we validated that MSRB3 was significantly up-regulated in ccRCC samples and cell lines. It was also demonstrated that the up-regulation of MSRB3 was associated with several clinicopathologic features. Knockdown of MSRB3 remarkably arrested the proliferation, migration and invasion, while promoted apoptosis, and induced the changes of markers of endoplasmic reticulum stress. Conclusion In conclusion, we demonstrated that MSRB3 was an oncogene of ccRCC associated with patients’ pathological characteristics and modulated endoplasmic reticulum stress of cancer cells.

BACKGROUND Prostate cancer (PCa), accounting for 28% of all male cancer cases, is the second leading cause of cancer-related death among men. NFATc1, belonging to the NFAT family, is overexpressed in PCa and is correlated with the risk of recurrence after radical prostatectomy. MATERIAL AND METHODS In the present study, the expression of NFATc, c-myc, and PKM2 in PCa cells was regulated by lentiviruses and then detected by real-time PCR and Western blot analysis. Further, proliferation, invasion, and migration assays were performed. The glucose consumption and lactate production were assessed by biochemical detection. RESULTS We found that NFATc1 down-regulation significantly suppressed the proliferation and Warburg effect of PCa cells, concurrent with a decrease of c-myc and PKM2 expression. Likewise, the abilities of migration and invasion were also inhibited in NFATc1-silenced PCa cells. In addition, NFATc1 down-regulation-induced inhibition of cell proliferation, migration, invasion, and Warburg effect were counteracted by up-regulation of c-myc or PKM2. The expression of PKM2 was positively regulated by NFATc1 and c-myc expression. CONCLUSIONS These results indicate that NFATc1 down-regulation can suppress the proliferation, Warburg effect, and migration and invasion abilities of PCa cells, probably by regulating c-myc and PKM2 expression. NFATc1 may be a potential therapeutic target for PCa and could be used as a diagnosis or prognosis indicator of PCa.

MicroRNA-21 (miRNA-21), a kind of short, noncoding RNAs, functioned as a tumor marker and was upregulated in renal cell carcinoma (RCC). However, the underlying mechanisms of miRNA-21 in RCC were uncertain. Therefore, the effects and mechanisms of miRNA-21 on the proliferation, differentiation, and apoptosis of cultured human RCC cells were further investigated in this study. After slicing miRNA-21 in RCC cells, the viability, mRNA expression of C/EBPα and PPARγ, caspase 3 activity, and protein expression of mTOR, STAT3, and pSTAT3 were determined. It was found that knockdown of miRNA-21 downregulated the optical density (OD) value of cells, inhibited mRNA expression of PPARγ and C/EBPα, and enhanced activity of caspase 3. Furthermore, protein expression of pSTAT3 was also decreased in the absence of miRNA-21. Notably, miRNA-21-changed proliferation, differentiation, and apoptosis of human RCC cells were partially regulated following the block of the mTOR-STAT3 signaling pathway by the mTOR inhibitor (XL388). It was indicated that miRNA-21 promoted proliferation and differentiation and decreased apoptosis of human RCC cells through the activation of the mTOR-STAT3 signaling pathway.

External field plays a very important role in the interaction between the π-electron transition and atomic vibration of polyenes. It has significant effects on both the Huang–Rhys factor and the electron–phonon coupling. In this paper, the visible absorption and resonance Raman spectra of all- trans -β-carotene are measured in the 345–295 K temperature range and it is found that the changes of the 0–1 and 0–2 vibration bands of the absorption spectra with the temperature lead to the different electron–phonon coupling of fundamental, overtone, and combination modes. The electron-phonon coupling constants of all the modes are calculated and analyzed under different temperatures. The variation law of the electron–phonon coupling with the temperature well interprets the changes of the resonance Raman spectra, such as the shift, intensity and line width of the overtone and combination modes, which are all greater than those of the fundamental modes.

355 nm pulsed laser is employed to excite pre-resonance forward stimulated Raman scattering (FSRS) of liquid water at ambient temperature. Due to the shockwave induced dynamic high pressure, the obtained Raman spectra begin to exhibit double peaks distribution at 3318 and 3373 cm−1 with the input energy of 17 mJ,which correspond with OH stretching vibration with strong and weak hydrogen (H) bonds. With laser energy rising from 17 to 27 mJ, the Stokes line at 3318 cm−1 shifts to 3255 and 3230 cm−1 because of the high pressure being enlarged. When the energy is up to 32 mJ, only 3373 cm−1 peak exists. The strong and weak H bond exhibit quite different energy dependent behaviors.

The ν1-ν18a Fermi resonance (FR) of phenol were investigated by pressure-dependent Raman spectroscopy from atmospheric up to P=15.2GPa and temperature-dependent Raman spectroscopy from 40 down to T=-180°C, respectively. In the case of pressure, we found the Fermi coupling coefficient W, which were calculated based on the FR theory, exposed a value turnover between 1.912 and 2.244GPa in the process of increasing the pressure. This turnover phenomenon of the Fermi coupling coefficient W has been ascribed to the crystal structure of phenol evolving towards a more symmetric structure with pressure, from a structure like a pseudo-threefold helical chain at ambient pressure to like a ribbon arrangement at 1.912GPa, then to adopt a herringbone arrangement at much higher pressure. On the other hand, we also found the Fermi coupling coefficient W exhibited monotonic reduction without turnover points appearing by decreasing the temperature. The tendencies of the Fermi coupling coefficient W with temperature were in good agreement with the pressure dependence of the Fermi coupling coefficient W in the region of ambient to 1.912GPa, indicating that the effect of pressure and temperature on the FR of phenol in this region might be the same. A conformation evolving induced by pressure and temperature on the ν1 and ν18a FR of phenol have been analyzed.