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OBJECTIVE: This study aimed to investigate the relationship between serum levels of CXC subfamily chemokine 13 (CXCL13) and clinical outcomes following radical surgery for cervical cancer. PATIENTS AND METHODS: A total of 70 cervical cancer patients admitted to our hospital between August 2021 and December 2022 were selected as the study group, while 30 healthy individuals who underwent regular physical examinations during the same period were selected as the control group. The levels of CXCL13 were measured in both groups, and a comparison was made between pre- and post-operative CXCL13 levels in the study group and the control group. Follow-up data on clinical outcomes were collected for the study group, and clinical data were compared between the recurrence/metastasis group and the non-recurrence/metastasis group. Logistic regression analysis was performed to identify factors influencing recurrence and metastasis by incorporating variables showing significant differences. Additionally, Pearson's correlation analysis was used to examine the relationship between CXCL13 and clinical data. RESULTS: Postoperative levels of CXCL13 in the study group showed a significant decrease compared to preoperative levels, and they were lower than those in the control group (p<0.05). Among the 70 patients in the study group, 23 experienced recurrence or metastasis, while 47 did not. Significant differences were observed between the recurrence/metastasis group and the non-recurrence/metastasis group in terms of histological grade, depth of cervical invasion, FIGO stage, parametrial infiltration, lymph node metastasis, and CXCL13 (p<0.05). Logistic regression analysis revealed that CXCL13, histological grade, depth of cervical invasion, FIGO stage, parametrial infiltration, and lymph node metastasis were all factors influencing recurrence and metastasis. There was a positive correlation between CXCL13 and histological grade, depth of cervical invasion, FIGO stage, parametrial infiltration, and lymph node metastasis (p<0.05). CONCLUSIONS: The level of CXCL13 is closely associated with the clinical outcome of cervical cancer after radical surgery and can serve as an important indicator for predicting clinical outcomes. Its application in clinical practice is highly recommended. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the expressions of miR-151a-5p and miR-23b in lung cancer tissues and their effects on the biological functions of lung cancer A549 cells. PATIENTS AND METHODS: Samples of lung cancer tissue (55 cases) and pericarcinomatous tissue (55 cases) were collected in thoracic surgery in our hospital from May 2017 to November 2018. The expression levels of miR-151a-5p and miR-23b in lung cancer tissues and pericarcinomatous tissues were detected by RT-PCR. Lung cancer cells A549 were transfected. Before transfection, the cells were divided into a negative control group (NC group, transfected with miRNA NC), a group transfected with miR- 151a-5p inhibitor and a group transfected with miR-23b inhibitor. MTS Cell Proliferation Colorimetric Assay Kit (CCK8) was used to detect cell proliferation and draw the growth curve. Transwell chamber was used to detect the invasion ability in vitro, and BD flow cytometry was used to detect apoptosis in each group. RESULTS: The expression levels of miR-151a- 5p and miR-23b in lung cancer tissues were significantly higher than those in pericarcinomatous tissues (p<0.001). After 48 h to 72 h, the cell growth of both the miR-151a-5p inhibitor group and the miR-23b inhibitor group was significantly lower than that of the NC group (p<0.001). The numbers of invasion of miR-151a-5p inhibitor group and miR-23b inhibitor group were significantly lower than that of NC group (p<0.00). The apoptosis rates of miR-151a-5p inhibitor group and miR-23b inhibitor group were significantly higher than that of NC group (p<0.001). CONCLUSIONS: Both miR-151a-5p and miR- 23b are highly expressed in lung cancer, and the inhibition of miR-151a-5p and miR-23b can restrain the proliferation, invasion and migration of lung cancer A549 cells, thereby promoting the apoptosis of lung cancer A549 cells. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Several studies demonstrated that aberrant lncRNA expression contributes to cervical cancer (CC) development and progression. LINC00152, a novel lncRNA, has been identified as an oncogene involved in various cancers. In the present study, we aim to investigate the expression pattern, clinical significance, potential functional roles, and regulatory mechanism of LINC00152 in CC. PATIENTS AND METHODS: The transcription levels of LINC00152, miR-216b-5p, and HOXA1 in CC tissues and cell lines were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). LINC00152 knockdown in CC cells was conducted by transfecting the LINC00152-specific siRNA. The cell proliferation ability was evaluated by the Cell Counting Kit-8 (CCK-8) assay. Cell cycle and apoptosis analysis were assessed by flow cytometry. The target relation among LINC00152, miR-216b-5p, and HOXA1 were measured using the dual-luciferase reporter assay. The protein levels of HOXA1 in CC cells were determined by Western blot. RESULTS: LINC00152 was up-regulated in CC tissues and cell lines. The high expression level of LINC00152 was positively correlated with poor prognosis and histologic grade in CC. The silence of LINC00152 could inhibit the proliferation of CC cells through inducing the cell cycle arrest at G0/G1 phase and promote apoptosis in vitro. Mechanically, we demonstrated that LINC00152 could modulate the proliferation of CC cells through elevating HOXA1 expression level via sponging miR-216b-5p based on bioinformatics analysis and experimental validation. CONCLUSIONS: Our findings revealed a novel molecular mechanism underlying LINC00152 modulating CC progression through the miR-216b-5p/HOXA1 pathway, suggesting that LINC00152 might potentially act as an effective diagnostic marker and therapeutic target for cervical cancer. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the influence of the TOLL-like receptor 4 (TLR4)-mediated p38MAPK signaling pathway on chronic intermittent hypoxic (CIH)-induced oxidative stress and inflammatory cytokines in rats. MATERIALS AND METHODS: A total of 120 healthy male Sprague Dawley (SD) rats, aged between 8-10 weeks, were randomly divided into 9 groups (normoxia control group, CIH 2 weeks group, CIH 4 weeks group, CIH 6 weeks group, CIH 8 weeks group, CIH 6 weeks + p38MAPK receptor inhibit group, CIH 6 weeks + Tempol group, CIH 8 weeks + p38MAPK receptor inhibitor group and CIH 8 weeks + Tempol group). The expression of TLR4 and p38MAPK in the adipose tissue was evaluated, as well as the level of serum oxidative stress markers (SOD, TRx-1, MDA) and inflammatory cytokines (adiponectin, TNF-α, hsCRP and IL-6). RT-PCR and Western-blot were conducted to detect the expression of TLR4 and p38MAPK mRNA. RESULTS: W ith i ncreased h ypoxia, t he l evels of SOD and adiponectin in the serum of the CIH group decreased significantly, and the levels of TNF-α, hsCRP, IL-8 and IL-6 in serum increased significantly. After the intervention of antioxidant Tempol and p38MAPK inhibitor SB203580, SOD increased significantly but with significant MDA reduction. The levels of TNF-α, hsCRP, IL-8 and IL- 6 in serum significantly decreased. The results of RT-PCR and Western-Blot indicated that the P-p38 and TLR4 proteins related to the MAPK pathway were expressed in rat adipose tissue. With the hypoxia intensity, expression of P-p38 decreased after initially increasing. The expression of TLR4 showed a continuously growing trend. After Tempol treatment, the expression of p38MAPK protein decreased, and the expression of TLR4 did not change significantly, indicating the inhibiting effect of Tempol on p38MAPK, without a significant inhibiting effect on TLR4. CONCLUSIONS: The TLR4-mediated p38MAPK signaling pathway was active in adipose tissue and the expression of the corresponding molecules increased as the duration of intermittent hypoxia increased. The expression of TLR4 and p38MAPK components regulated the level of oxidative stress and inflammatory cytokines; the application of p38MAPK inhibitors and antioxidant free radical scavengers improved the levels of oxidative stress and inflammatory cytokines. [ABSTRACT FROM AUTHOR]