ABSTRACT
BACKGROUND: Many studies have investigated the prognostic role of the C-reactive protein/albumin ratio (CRP/Alb ratio) in patients with gynecological cancers; however, there is lack of consensus owing to conflicting results across studies. We performed a meta-analysis to determine the prognostic role of the CRP/Alb ratio in gynecological cancers. METHODS: We searched the PubMed, Embase, the Web of Science, Cochrane Library, China National Knowledge Infrastructure, and Wanfang electronic databases since inception to April 2021. Combined hazard ratios (HRs) and 95% confidence intervals (CIs) were used to estimate the prognostic effect of the CRP/Alb ratio in gynecological cancers. Pooled odds ratios (ORs) and 95% CIs were used to investigate the association between the CRP/Alb ratio and clinicopathological features. RESULTS: The meta-analysis included seven studies with 1,847 patients. The pooled results showed that a high pretreatment CRP/Alb ratio was associated with poor overall survival (HR, 1.84; 95% CI, 1.41-2.40; p < 0.001) and progression-/disease-free survival (HR, 2.58; 95% CI, 1.42-4.68; p = 0.002). Additionally, a high CRP/Alb ratio was significantly associated with stages III-IV disease (the International Federation of Gynecology and Obstetrics classification) (OR, 2.98; 95% CI, 1.45-6.14; p = 0.003). However, we observed a non-significant correlation between the CRP/Alb ratio and lymph node metastasis, tumor size, and histopathological grade. CONCLUSIONS: The CRP/Alb ratio is a convenient and accurate predictor of survival outcomes in gynecological cancers. A high CRP/Alb ratio also predicts tumor progression.
ABSTRACT
BACKGROUND: Integrin ß6 (ITGB6), a key submonomer of integrin αvß6, plays an important role in epithelial-to-mesenchymal transition (EMT), wound healing, epithelial-derived tumor growth, fibrosis, and epithelial repair. However, the role of ITGB6 in cervical carcinoma (CC) remains elusive. METHODS: The expression levels of ITGB6 in CC tissues and cell lines were determined using quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability, proliferation, apoptosis, migration, and invasion were evaluated by Cell Counting Kit-8 (CCK-8), colony-forming, flow cytometry, and Transwell assay, respectively. The expression of related proteins, including EMT markers and the Janus kinase/signal transducer and activator of transcription (JAK/STAT3) signaling markers, were detected using western blotting. RESULTS: The ITGB6 expression in CC tissues and cells (C-33A, Hela, SiHa, and Caski) was remarkably higher than that in paracarcinoma tissues and ECT1/E6E7 cells. The data from The Cancer Genome Atlas (TCGA) data set suggested that patients with CC with high ITGB6 expression showed poorer overall survival (OS). Compared with the empty transfection group (si-NC), si-ITGB6 restrained the proliferation, migration, and invasion of SiHa and Hela cells, while promoting cell apoptosis. si-ITGB6 suppression decreased the expression of Snail, vimentin, and N-cadherin, while increasing E-cadherin expression. Further research showed that si-ITGB6 reduced p-JAK1/JAK1, p-JAK2/JAK2, and p-STAT3/STAT3 expression in the JAK/STAT3 signaling pathway. Interestingly, proliferation, migration, invasion, and the expressions of the molecular markers of the JAK/STAT3 signaling pathway and EMT pathway induced by ITGB6 were altered by RO8191 (JAK/STAT3 pathway activator). Furthermore, the protein expression levels of Snail, vimentin, N-cadherin, p-STAT3/STAT3, p-JAK1/JAK1, and p-JAK2/JAK2 in tumor tissues were higher than those in adjacent normal tissue, while the expression level of E-cadherin was downregulated in tumor tissues. CONCLUSIONS: Silencing of ITGB6 restrains cell proliferation, migration and invasion, and promotes apoptosis in CC by inhibiting JAK/STAT signaling pathways. Thus, ITGB6 may perhaps be a new and useful candidate target for treating CC.
ABSTRACT
BACKGROUND: Early detection and diagnosis of ovarian cancer (OC) is complicated due to the concealment of the ovarian anatomical position and the lack of clinical manifestations and specific indicators of early OC. Therefore, it is urgent to study the pathogenesis of OC, especially the molecular mechanism. RESULTS: LncRNA GAS8-AS1 was decreased in OC tissues and cell lines, and high expression of GAS8-AS1 indicated a higher 5-year survival rate of OC patients. Overexpression of GAS8-AS1 suppressed growth of OC cells, while deletion of GAS8-AS1 promoted the progression of OC cells. Further data indicated GAS8-AS1 activated autophagy in OC cells. Functional experiments showed that 3-MA removed the inhibitory effect of GAS8-AS1 in OC cells. On the contrary, Rapamycin reversed the promoting effect of GAS8-AS1 in OC cells. Furthermore, GAS8-AS1 bound with Beclin1 and promoted its expression, and silencing of Beclin1 reversed the inhibitory role of GAS8-AS1 in OC progression. In vivo tumorigenesis assay showed GAS8-AS1 suppressed OC progression and activated Beclin1 mediated autophagy. CONCLUSION: Our study suggested GAS8-AS1 inhibited OC progression by activating autophagy via binding with Beclin1, and GAS8-AS1 might be a potential therapeutic target for OC clinical treatment.