Abstract
Introduction: Aberrant activation of Semaphorin3C(SEMA3C) is widespread in human cancers. We aimed to analyze SEMA3C expression in cervical cancer and investigate the role of SEMA3C in cervical cancer and its underlying mechanism, which is important for exploring new therapeutic targets and prognostic factors.Materials and Methods: The expression of SEMA3C was examined in paraffin-embedded cervical cancer specimens. In vivo and in vitro assays were performed to validate the effect of SEMA3C on cervical cancer cell proliferation and p-ERK pathway activation. Gene Set Enrichment Analysis (GSEA) was performed using The Cancer Genome Atlas (TCGA) data set.Results: SEMA3C expression was associated with poor survival in both the TCGA cohort and our cohort. Silencing of SEMA3C suppressed cervical cancer cell proliferation, colony formation ability, and the activation of the p-ERK signaling pathway in vitro. SEMA3C depletion inhibited tumor growth in vitro. GSEA also showed that the epithelial mesenchymal transition (EMT), TGFβ signaling pathway, angiogenesis, and extracellular matrix (ECM) receptor interactions are associated with a high SEMA3C expression phenotype.Conclusion: SEMA3C is correlated with poor prognosis of cervical cancer patients and promotes tumor growth via the activation of the p-ERK pathway.
Highlights
Aberrant activation of Semaphorin3C(SEMA3C) is widespread in human cancers
We evaluated SEMA3C expression by IHC in 87 human cervical cancer samples
The patients in the TCGA cohort were divided into two groups according to the cutoff representing the value that yields maximal difference, and the expression of SEMA3C mRNA was high in 201/304 analyzed samples and low in 103/304 samples
Summary
Aberrant activation of Semaphorin3C(SEMA3C) is widespread in human cancers. We aimed to analyze SEMA3C expression in cervical cancer and investigate the role of SEMA3C in cervical cancer and its underlying mechanism, which is important for exploring new therapeutic targets and prognostic factors. Cervical cancer is one of the most common gynecological cancers with 570,000 new cases and 311,000 deaths per year worldwide [1]. Despite the preventive vaccine for HPV, which is promising for reducing cervical cancer cases in the future, the coverage rates are still low due to the high price currently, especially in low- and middle-income countries [3]. The global incidence of cervical cancer has increased at a 0.6% annual rate over the past few decades [4]. Unraveling the molecular mechanisms of cervical cancer is still critical and may provide disease-specific opportunities for therapeutic. Identifying prognostic biomarkers for cervical cancer patients may be conducive to selecting suitable follow-up intervals and subsequent therapies
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
