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The development of medical detection, storage, and other technologies makes China’s medical and health field accumulate massive data. Big data analysis technology can mine and analyze these data and establish medical information systems to enhance hospital treatment and service levels. Therefore, this work studies the construction and application of medical economic information systems. Specifically, neural networks, as a means to handle a large number of medical economic data, and has received great attention. This work uses BP neural network to extract the medical economic information feature, which is a big data technology and can extract deep features of data, after that, we compare and analyze the characteristic of different medical data. Finally, we establish the medical economic information system for the follow-up medical diagnostic services.

Purpose This study aimed to investigate the effects of microRNA (miR)-22 on biological behaviors of colon cancer cells and to explore the relationship between miR-22 and NLRP3. Materials and Methods First, human colon cancer HCT116 cells were transfected with a miR-22 mimic, miR-22 inhibitor, control mimic, and control inhibitor, respectively. CCK8, colony formation, and transwell assays were performed to observe cell proliferation, migration, and invasion. Western blotting was used to analyze the expression of recombinant NLRP3 (NLR family, pyrin domain-containing protein 3) and epithelial-mesenchymal transformation (EMT)-related proteins. The target relationship between miR-22 and NLRP3 was verified by double luciferase report. Second, an NLRP3 inhibitor and NLRP3 mimic were transfected into HCT116 cells, and the biological behaviors and EMT-related proteins were again observed. Finally, a nude mouse xenograft model was constructed to verify the above results. Results In vitro, compared with the control group, administration of the miR-22 mimic significantly decreased proliferation, migration, and invasion of HCT116 cells, whereas the miR-22 inhibitor markedly increased their proliferation and invasion (p

Introduction Sineoculis homeobox homolog 1 (Six1) overexpression has been implicated in several human cancers. To date, its clinical significance and potential function in human thyroid cancer remain unclear. Methods Immunohistochemistry was used to examine the protein expression of BCAT1 in 89 cases of thyroid cancer tissues. We overexpressed and knockdown Six1 in TPC-1 and B-CPAP thyroid cancer cell lines. Biological roles and potential mechanisms of Six1 were examined using CCK-8, colony formation assay, Matrigel invasion assay, Western blot, PCR, ATP assay, and 2-NBDG uptake assay. Results We showed that Six1 protein was upregulated in thyroid cancers and was associated with tumor size and nodal metastasis. Analysis of TCGA dataset indicated that Six1 mRNA was higher in thyroid cancers compared with normal thyroid. CCK-8, colony formation and Matrigel invasion assays demonstrated that Six1 overexpression promoted proliferation, colony number and invasion while Six1 siRNA knockdown inhibited the growth rate, colony formation ability and invasive ability in both cell lines. Notably, Six1 upregulated glucose consumption, lactate production level and ATP level. 2-NBDG uptake analysis showed that Six1 overexpression upregulated glucose uptake while Six1 knockdown inhibited glucose uptake. Further analysis revealed that Six1 overexpression upregulated Snail, MMP2 and GLUT3 at both mRNA and protein levels. TCGA analysis demonstrated positive associations between Six1 and Snail, MMP2 and GLUT3 at the mRNA levels. Conclusion Taken together, our data demonstrated that Six1 was upregulated in human thyroid cancers and promoted cell proliferation and invasion. Our data also revealed new roles of Six1 in thyroid cancer development by modulating glucose metabolism and invasion, possibly through regulation of Snail, MMP2 and GLUT3.

Heparanase (HPSE) is an endo-β-D-glucuronidase overexpressed in different types of human cancer, and a predicted target of microRNA (miRNA/miR)-219a-2-3p in thyroid cancer. The present study aimed to investigate the potential role of HPSE and miR-219a-2-3p in thyroid cancer, and the molecular mechanism of miR-219a-2-3p regulating the proliferation of thyroid cancer cells via HPSE was confirmed. Immunohistochemistry analysis was performed to detect HPSE expression in thyroid cancer sections. In addition, reverse transcription-quantitative PCR analysis was performed to detect mRNA and miR-219a-2-3p expression levels in thyroid cancer samples and cell lines. miR-219-2-3p mimic or HPSE plasmid were transfected into B-CPAP and TPC-1 thyroid cancer cells. Furthermore, western blot analysis was performed to detect the protein expression levels of HPSE and cyclin D1. Cell cycle analysis was performed using propidium iodide staining and flow cytometry, and EdU incorporation was performed to detect cell proliferation. The results demonstrated that high HPSE expression was significantly associated with tumor size, extracapsular invasion and lymph node metastasis. Notably, a statistically negative correlation was observed between HPSE mRNA expression and miR-219a-2-3p expression in thyroid cancer tumors, as well as in thyroid cancer cell lines. When exogenously expressed in B-CPAP and TPC-1 cells, miR-219a-2-3p induced cell cycle arrest at the G(0)/G(1) phase and decreased the percentage of proliferating cells. Furthermore, HPSE and cyclin D1 protein expression decreased following transfection with miR-219a-2-3p. Notably, when HPSE was ectopically expressed in miR-219a-2-3p transfected cells, cyclin D1 expression and the number of proliferative cells increased. Taken together, these results suggest that HPSE contributes to the proliferation of thyroid cancer cells. In addition, miR-219a-2-3p was confirmed to target HPSE and inhibit cell proliferation, which was associated with cyclin D1 suppression-mediated cell cycle arrest.

Additional file 1: Supplementary Figure 1. The original blots of Ki-67, FUT4, β-catenin, Cyclin D1, p-GSK-3β, GSK-3β in Lovo and SW480 cells. (Corresponding to Fig. 6 in the manuscript).

Additional file 2: Supplementary Figure 2. The original blots of Ki-67, FUT4, β-catenin, Cyclin D1, p-GSK-3β, GSK-3β in Lovo and SW480 cells. (Corresponding to Fig. 8 in the manuscript).

Background MicroRNA (miR)-200c has been widely reported to be involved in colon cancer progress. However, the mechanisms of miR-200c in regulating tumor metastasis and growth remain to be fully elucidated. This study aimed to investigate the mechanism of miR-200c targets fucosyltransferase 4 (FUT4) on the proliferation of colon cancer. Methods The miR-200c and FUT4 mRNA levels in LoVo and SW480 cells were measured by real-time quantitative polymerase chain reaction. Further, miR-200c mimic, FUT4 siRNA and FUT4 mimic were transfected into cells, separately. Cell counting kit-8, plate colony formation and transwell assays were used to analyse the cells biological behaviour.. Immunofluorescence was used to analyse the Ki-67 expression Moreover, the Wnt/β-catenin pathway-related proteins were detected by western blots. A double luciferase experiment was performed to confirm the relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin pathway-related proteins were also analysed. Results In vitro, the expression of miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were − 0.9046 and − 0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo and SW480 cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A dual luciferase reporting system identified FUT4 as the target of miR-200c. The results in vivo were further confirmed the foundation of cells study. Conclusions In summary, miR-200c overexpression inhibits proliferation of colon cancer targeting FUT4 to downregulate the Wnt/β-catenin pathway, which promises molecular targets to inhibit metastasis for colon cancer therapy.

BackgroundTo investigate the effects of miR-200c, which targets fucosyltransferase 4 (FUT4), on the proliferation, migration and invasion of colon cancer cells and to further explore its mechanism.MethodsWe assessed the miR-200c and FUT4 mRNA levels in LoVo and SW480 cells by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analysed by Pearson correlation analysis. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into LoVo and SW480 cells, and RT-PCR was used to analyse the transfection efficiency. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to detect the migration, invasion and proliferation of LoVo and SW480 cells. Immunofluorescence was used to analyse the expression of the Ki-67 protein. Moreover, the expression of Wnt/β-catenin signalling pathway-related proteins was detected by western blots. A double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin signalling pathway-related proteins were also analysed. ResultsPearson correlation analysis showed that miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A bioinformatics analysis and a dual luciferase reporting system identified FUT4 as the target of miR-200c. ConclusionsIn conclusion, miR-200c overexpression inhibits FUT4 expression and downregulates the Wnt/β-catenin signalling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

Background Heparanase (HPSE) is an endo-β-D-glucuronidase, which is found overexpressed in various human cancers. The purpose of our work was to investigate the possible role of HPSE and the involved signaling molecules in the development of papillary thyroid carcinoma (PTC). Methods The expression of HPSE was examined in 80 samples of PTC by immunohistochemistry. In cell studies, the expression plasmid of HPSE and RNA interference with shRNA specific for HPSE were used to elucidate the effects of HPSE on proliferation, apoptosis, migration and invasion in PTC cells of B-CPAP and KTC-1. The probable downstream signaling molecules of HPSE were also explored. Results 75.0% (60 out of 80) of PTC samples was detected high expression of HPSE, which was significantly correlated with tumor size, lymph node metastasis and stage status. In cell studies, the upregulation of HPSE significantly promoted cell proliferation, migration and invasion of B-CPAP and KTC-1 cells, and interfered with cell apoptosis. On the contrary, knockdown of HPSE exhibited the opposite effects. Compared with the parental cells, HPSE silencing cells showed attenuated capabilities of proliferation, migration and invasion, yet the apoptotic rate of transfected cells was increased. The activations of various signaling molecules correlated with cell biological behavior were found to be regulated by HPSE upregulation or knockdown. Conclusions Our results suggested that HPSE probably contributed to the progression and metastasis of PTC, which were associated with multiple signaling pathways. HPSE could be a potent molecular target for the therapeutic strategy of PTC.

Background To investigate the effects of miR-200c targeting fucosyltransferase 4 (FUT4) on the proliferation, migration and invasion of colon cancer cells and further to explore its mechanism. Methods The expression of miR-200c and FUT4 mRNA in Lovo and SW480 cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analyzed by Pearson. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into Lovo and SW480 cells, and RT-PCR was used to analyze the effect of transfection. Cell counting kitcck-8 (CCK-8), cloning and transwell assays were used to detect the migration, invasion and proliferation of Lovo and SW480 cells, respectively. Immunofluorescence was used to analyze the expression of Ki-67 protein. Moreover, the expression of Wnt/β-catenin signaling pathway-related proteins were detected by western blot. Double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. Results Pearson results showed that miR-200c and FUT4 were negatively correlated in Lovo and SW480 cells (correlation coefficients were − 0.9046 and − 0.9236, respectively). MiR-200c overexpression inhibits the proliferation, migration and invasion of Lovo cells by down-regulating FUT4. The expression of Ki67 positive cells and Wnt/β-catenin signaling pathway-related proteins were reduced in miR-200c overexpression and FUT4 silencing groups. The scientific search and dual luciferase reporting system identified FUT4 was the target of miR-200c. Conclusion In conclusion, miR-200c overexpression inhibits FUT4 expression and down-regulates the Wnt/β-catenin signaling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

Expressed on cells of the myeloid and lymphoid lineages, V-domain Ig Suppressor of T cell Activation (VISTA) is an emerging target for cancer immunotherapy. Blocking VISTA activates both innate and adaptive immunity to eradicate tumors in mice. Using a tripeptide small molecule antagonist of VISTA CA170, we found that it exhibited potent anticancer efficacy on carcinogen-induced mouse lung tumorigenesis. Remarkably, lung tumor development was almost completely suppressed when CA170 was combined with an MHCII-directed KRAS peptide vaccine. Flow cytometry and single-cell RNA sequencing (scRNA-seq) revealed that CA170 increased CD8+ T cell infiltration and enhanced their effector functions by decreasing the tumor infiltration of myeloid-derived suppressor cells (MDSCs) and Regulatory T (Treg) cells, while the Kras vaccine primarily induced expansion of CD4+ effector T cells. VISTA antagonism by CA170 revealed strong efficacy against lung tumorigenesis with broad immunoregulatory functions that influence effector, memory and regulatory T cells, and drives an adaptive T cell tumor-specific immune response that enhances the efficacy of the KRAS vaccine., Pan, Chen, Zhang et al. investigated the anti-cancer efficacy of CA170, a small molecule agonist of VISTA, on mouse lung tumorigenesis. When combined with a MHCII-directed KRAS peptide vaccine, the authors reported that CA170 suppressed lung tumor development by increasing CD8+ T cell and decreasing MDSC and Treg infiltration, while the Kras vaccine induced CD4+ effector T cell expansion

Background To investigate the effect of the cell proliferation, migration and invasion in human colon cancer cells which based on the mechanism of miR-22 targeting NLR family pyrin domain containing3(NLRP3) Methods Human colonic epithelial cells (HCoEpiC) and human colon cancer cell lines (HCT116, HCT8, HT29, LS174T, LOVO, SW480) were prepared for the present study. The HCT116 cells were divided into 2 parts with different processes, and each part was randomly divided into different groups (part1: BC, NC1, miR-22, NC2, si-miR and part2: BC, miR-22, NC3, si-NLRP3, miR + NC4, miR + NLRP3). Quantification the expression levels of miR-22, NLPR3 and miR-22 targeting NLRP3 related proteins by means of qRT-PCR and Western blot. The colon cancer cell proliferation, invasion and migration were assessed via CCK8, colony formation and transwell assays. Subsequently, nude xenografts mice model was constructed and mice were divided into 4 groups: Model, miR-22, si-NLRP3 and miR + NLRP3. Through the changes of tumor volume and weight, the expression of Ki67 and the protein levels of NLRP3, IL-1B, MMP-9, MMP-2, E-catherine, N-catherine and Vimentin to verify the results. Results The cell proliferation, migration and invasion in miR-22, si-NLRP3 and miR + NLRP3 groups were significantly weaker than BC group. In compared to normal tissues, the growth rate of tumor was evidently slowed down, the volume and quality of tumor were evidently reduced and the proportion of Ki67 positive cells were evidently decreased. Both in tumor tissues and in cancer cells, the expression of IL-1B, NLRP3, MMP-9, MMP-2, N-Catherine and Vimentin were evidently decrease and the levels of E-Catherine were evidently increased than in normal tissues or cells. In compared to si-miR and CYLD groups, treatment with si-miR + si-C could effectively reverse the effect of suppressed the tumor progression. Conclusion miR-22 targets NLRP3 to inhibit the cell proliferation, migration and invasion in human colon cancer cell

Purpose This study aimed to investigate the effects of microRNA (miR)-22 on biological behaviors of colon cancer cells and to explore the relationship between miR-22 and NLRP3. Materials and Methods First, human colon cancer HCT116 cells were transfected with a miR-22 mimic, miR-22 inhibitor, control mimic, and control inhibitor, respectively. CCK8, colony formation, and transwell assays were performed to observe cell proliferation, migration, and invasion. Western blotting was used to analyze the expression of recombinant NLRP3 (NLR family, pyrin domain-containing protein 3) and epithelial–mesenchymal transformation (EMT)-related proteins. The target relationship between miR-22 and NLRP3 was verified by double luciferase report. Second, an NLRP3 inhibitor and NLRP3 mimic were transfected into HCT116 cells, and the biological behaviors and EMT-related proteins were again observed. Finally, a nude mouse xenograft model was constructed to verify the above results. Results In vitro, compared with the control group, administration of the miR-22 mimic significantly decreased proliferation, migration, and invasion of HCT116 cells, whereas the miR-22 inhibitor markedly increased their proliferation and invasion (p

To characterize the somatic alterations of papillary thyroid carcinomas (PTC) in Chinese patients, we performed the next-generation-sequencing (NGS) study of the tumor-normal pairs of DNA and RNA samples extracted from 16 Chinese PTC patients. The whole genome sequencing (WGS) and transcriptome sequencing (RNA-seq) were conducted for 6 patients who were either current or former smokers and the whole exome sequencing (WES) and RNA-seq were conducted for another 10 patients who were never smokers. The NGS data were analyzed to identify somatic alteration events that may underlie PTC in Chinese patients. We identified a number of PTC driver genes harboring somatic driver mutations with significant functional impact such as COL11A1, TP53, PLXNA4, UBA1, AHNAK, CSMD2 and TTLL5 etc. Significant driver pathways underlying PTC were found, namely, the metabolic pathway, the pathway in cancer, the olfactory transduction pathway and the calcium signaling pathway. In addition, this study revealed genes with significant somatic copy number aberrations and corresponding somatic gene expression changes in PTC tumors, the most promising ones being BRD9, TRIP13, FZD3, and TFDP1 etc. We also identified several structural variants of PTCs, especially the novel in-frame fusion proteins such as TRNAU1AP-RCC1, RAB3GAP1-R3HDM1, and ENAH-ZSWIM5. Our study provided a list of novel PTC candidate genes with somatic alterations that may function as biomarkers for PTC in Chinese patients. The follow-up mechanism studies may be conducted based on the findings from this study.

To better understand the etiology of papillary thyroid carcinoma, we did next-generation sequencing for the exomes and transcriptomes of a Chinese cohort of 28 pairs of DNA and RNA samples extracted from papillary thyroid carcinoma tumors and adjacent normal thyroid samples. The Chinese papillary thyroid carcinoma tumors harbored somatic mutations in the known driver genes, such as KRAS, TP53, BRAF, ERBB2, and MET. In addition, we identified novel papillary thyroid carcinoma candidate genes that had not been well studied before. We also identified a gene mutation signature involving SPTA1, MAP2, SYNE1, and SLIT3 that is significantly associated with survival of papillary thyroid carcinoma patients. Transcriptome analysis using the initial papillary thyroid carcinoma tumor samples and a new Chinese papillary thyroid carcinoma dataset identified six commonly upregulated oncogenic pathways in both datasets including eukaryotic translation initiation factor 2, phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K)/serine/threonine kinase (AKT), Ephrin Receptor, Rho Family GTPase signaling, nuclear factor, erythroid 2 like 2 (NRF2)-mediated oxidative stress response, and remodeling of epithelial adherens junctions. Overall, we identified novel candidate genes and oncogenic pathways important to the etiology of papillary thyroid carcinoma in Chinese patients and found the association of a gene signature with the survival outcome of the thyroid cancer patients. These findings may help in moving toward the more comprehensive and effective personalized treatment of papillary thyroid carcinoma in Chinese.

Background Heparanase (HPSE) is an endo-β-D-glucuronidase, which is found overexpressed in various human cancers. The purpose of our work was to investigate the possible role of HPSE and the involved signaling molecules in the development of papillary thyroid carcinoma. Methods In this study, the expression plasmid of HPSE and RNA interference with shRNA specific for HPSE were used to elucidate the effects of HPSE on proliferation, apoptosis, migration and invasion in papillary thyroid carcinoma cells of B-CPAP. The probable downstream signaling molecules of HPSE were also explored. Results The results showed that upregulation of HPSE significantly promoted cell proliferation, migration and invasion of B-CPAP cells, and interfered with cell apoptosis. On the contrary, knockdown of HPSE exhibited the opposite effects. Compared with the parental cells, HPSE silencing cells showed attenuated capabilities of proliferation, migration and invasion, yet the apoptotic rate of transfected cells was increased. The activations of various signaling molecules correlated with cell biological behavior were found to be regulated by HPSE upregulation or knockdown. Conclusions Our results suggested that HPSE probably contributed to the progression and metastasis of papillary thyroid carcinoma, which were associated with multiple signaling pathways. HPSE could be a potent molecular target for the therapeutic strategy of papillary thyroid carcinoma.

Papillary thyroid carcinoma (PTC) is an aggressive histological subtype of thyroid carcinoma (THCA), whose occurrence rate is high. The participation of long noncoding RNAs in the pathologies of cancers has attracted significant attention during the past decades. The purpose of the current study is to investigate the role of NR2F1 antisense RNA 1 (NR2F1-AS1) in PTC. The expression of NR2F1 in THCA samples was analyzed by bioinformatics tool gene expression profiling interactive analysis. Levels of NR2F1-AS1, microRNA-423-5p (miR-423-5p), and SRY-box 12 (SOX12) were evaluated by a quantitative reverse transcription-polymerase chain reaction and Western blot. The impact of NR2F1-AS1 on PTC cell proliferation and invasion was assessed by Cell Counting Kit-8, EdU, and Transwell invasion assays. The interactions among NR2F1-AS1, miR-423-5p, and SOX12 were determined by RNA immunoprecipitation and luciferase reporter assays. Consequently, we found that NR2F1-AS1 and SOX12 levels were elevated in PTC, whereas miR-423-5p was downregulated in PTC cells. Functionally, NR2F1-AS1 silence led to reduced proliferation and invasion of PTC cells. Mechanistically, NR2F1-AS1 interacted with miR-423-5p to induce SOX12 expression in PTC cells. In conclusion, the present study firstly stated that NR2F1-AS1 regulated miR-423-5p/SOX12 to promote proliferation and invasion of PTC, indicating NR2F1-AS1 as a potential novel target for the molecular-targeted therapy of PTC.

Immunotherapy using monoclonal antibodies to block immune checkpoints is becoming a mainstream therapy for multiple late-stage cancers owing to their efficacy in improving clinical outcomes. However, relatively low response rates and persistent clinical side effects indicate the need for additional strategies to block immune-suppressive pathways. VISTA (V-domain Ig Suppressor of T cell Activation), which is expressed on cells of the myeloid and lymphoid lineages, is an emerging target for cancer immunotherapy. Blocking VISTA activates both innate and adaptive immunity to eradicate tumors in mice. We found that CA170, a novel orally bioavailable tripeptide small molecule antagonist of VISTA and PD-L1/PD-L2, has potent anticancer efficacy on carcinogen-induced mouse lung tumorigenesis. Remarkably, lung tumor development was almost completely suppressed when CA170 was combined with an MHC-II-directed KRAS peptide vaccine. Flow cytometry and single cell RNA sequencing (scRNA-seq) revealed that CA170 increases CD8+ T cell infiltration and effector functions by decreasing the tumor infiltration of myeloid derived suppressor cells (MDSCs) and regulatory T cells (Tregs), while the KRAS vaccine primarily induces expansion of CD4+ effector T cells. Inhibition of VISTA by CA170 has strong efficacy against lung tumorigenesis with broad immunoregulatory functions that influence effector, memory and regulatory T cells, and promotes an adaptive T cell tumor-specific immune response that enhances efficacy of the KRAS vaccine. Citation Format: Jing Pan, Yao Chen, Qi Zhang, Achia Khatun, Katie Palen, Li Wang, Chuanjia Yang, Bryon D. Johnson, Charles R. Myers, Shizuko Sei, Robert H. Shoemaker, Ronald A. Lubet, Yian Wang, Weiguo Cui, Ming You. Inhibition of lung tumorigenesis by a novel small molecule CA170 targeting the immune checkpoint protein VISTA [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 1618.

To understand the genetic causes of pancreatic cancer (PC), we conducted a genome-wide association study (GWAS) using the diversity outbred (DO) mice population to identify susceptibility genes underlying 7,12-dimethylbenzanthraene (DMBA) induced PC. The phenotype studied was the percent PC lesion area in the DO mice population. We genotyped 7851 SNP markers specifically designed for DO mice across the whole mouse genome. Four susceptibility genes with P values exceeding the genome-wide threshold for percent PC lesion area (P

Summary SCC-S2 overexpression has been implicated in several human cancers, its correlation with prognosis and the mechanism how it reserved biological roles are still uncertain. The current study demonstrated that, in 142 archived colorectal carcinoma (CRC) tissue samples, SCC-S2 expression was significantly correlated with higher histological grade ( p=0.001), tumor invasion ( p=0.001), advanced Dukes staging ( p=0.002), positive regional lymph node metastasis ( p=0.024), and poor overall survival ( p

Supplemental material, DS_10.1369_0022155418799957 for SCC-S2 Facilitates Tumor Proliferation and Invasion via Activating Wnt Signaling and Depressing Hippo Signaling in Colorectal Cancer Cells and Predicts Poor Prognosis of Patients by Chuanjia Yang, Weixue Xu, Xiangzhen Meng, Siqi Zhou, Minglu Zhang and Dongxu Cui in Journal of Histochemistry & Cytochemistry