High expression of novel biomarker KRT16P3 promotes the progression of tongue squamous cell carcinoma and predicts poor prognosis

xloma.fota13 shared this article with you from Inoreader High expression of novel biomarker KRT16P3 promotes the progression of tongue squamous cell carcinoma and predicts poor prognosis Via Oral Pathology & Medicine Abstract Background Overexpression of long noncoding RNAs (lncRNAs) reveals the abnormal pathological processes in many human cancers. KRT16P3, a novel overexpressed lncRNA in tongue squamous cell carcinoma (TSCC), was identified by previous lncRNA microarrays. However, the role of KRT16P3 in TSCC is not clear. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to detect the expression of KRT16P3 in TSCC tissues and cells. Next, the relationships between KRT16P3 and the clinical significance of TSCC patients were analyzed. Additionally, Cell Counting Kit‐8, 5‐Bromo‐2‐deoxyUridine (BrdU) incorporation assay, cell colony formation assay, flow cytometry cell apoptosis analysis, scratch wound healing assay, transwell invasion assay were used to explore the biological function of KRT16P3. Western blot and qRT‐PCR were used to determine the expression of epithelial‐mesenchymal transition (EMT) markers. The pathway changes after KRT16P3 knockdown were detected by western blot. Results We found KRT16P3 expression is significantly upregulated in TSCC tissues and positively associated with advanced clinicopathological features of TSCC patients, and it may serve as a poor prognostic factor. Functionally, KRT16P3 knockdown inhibits proliferation, migration, invasion, and promotes apoptosis of TSCC cells. Furthermore, we also revealed that KRT16P3 knockdown supresses EMT and JAK2/STAT3 signaling pathway. Conclusion Our results validated that KRT16P3 can modulate the malignant progression, EMT process, and JAK2/STAT3 signaling pathway of TSCC, which might also serve as a novel prognostic biomarker and an attractive target for TSCC patients. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.