Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Beijing, China.
J Oral Pathol Med. 2021 Apr;50(4):385-393. doi: 10.1111/jop.13138. Epub 2021 Feb 3.
Overexpression of long non-coding 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.
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.
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 suppresses EMT and JAK2/STAT3 signaling pathway.
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.
长链非编码 RNA（lncRNA）的过表达揭示了许多人类癌症的异常病理过程。KRT16P3 是舌鳞状细胞癌（TSCC）中一种新的过表达 lncRNA，通过之前的 lncRNA 微阵列鉴定。然而，KRT16P3 在 TSCC 中的作用尚不清楚。
采用定量实时聚合酶链反应（qRT-PCR）检测 KRT16P3 在 TSCC 组织和细胞中的表达。接下来，分析 KRT16P3 与 TSCC 患者临床意义的关系。此外，使用细胞计数试剂盒-8（Cell Counting Kit-8）、5-溴-2-脱氧尿苷（BrdU）掺入测定、细胞集落形成测定、流式细胞术细胞凋亡分析、划痕愈合测定、Transwell 侵袭测定来探索 KRT16P3 的生物学功能。Western blot 和 qRT-PCR 用于确定上皮-间充质转化（EMT）标志物的表达。通过 Western blot 检测 KRT16P3 敲低后通路的变化。
我们发现 KRT16P3 在 TSCC 组织中的表达显著上调，并与 TSCC 患者的晚期临床病理特征呈正相关，它可能作为一个不良预后因素。功能上，KRT16P3 敲低抑制 TSCC 细胞的增殖、迁移和侵袭，并促进凋亡。此外，我们还揭示了 KRT16P3 敲低抑制 EMT 和 JAK2/STAT3 信号通路。
我们的研究结果验证了 KRT16P3 可以调节 TSCC 的恶性进展、EMT 过程和 JAK2/STAT3 信号通路，它也可能作为一种新的预后生物标志物和 TSCC 患者有吸引力的治疗靶点。
