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首页> 外文期刊>American Journal of Translational Research >Long non-coding RNA KRT16P2/miR-1294/EGFR axis regulates laryngeal squamous cell carcinoma cell aggressiveness
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Long non-coding RNA KRT16P2/miR-1294/EGFR axis regulates laryngeal squamous cell carcinoma cell aggressiveness

机译:长期非编码RNA KRT16P2 / MIR-1294 / EGFR轴调节喉鳞状细胞癌细胞侵略性

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Laryngeal squamous cell carcinoma (LSCC) is one of the most commonly seen head and neck malignancies. Identifying potent markers and/or targets for early diagnosis and individualized therapies for LSCC remains a considerable challenge. The present study analyzed online data and identified lncRNA KRT16P2 as a significantly upregulated long non-coding RNA (lncRNA) in LSCC. KRT16P2 knockdown in LSCC cells inhibited cancer cell proliferation, invasion, and migration. Similar to KRT16P2, EGFR expression was also significantly upregulated in LSCC. KRT16P2 and EGFR were positively correlated in LSCC tissue samples. EGFR knockdown also dramatically inhibited LSCC cell proliferation and aggressiveness (invasion and migration). Through online data and online tools, miR-1294 was predicted to target KRT16P2 and EGFR 3’UTR simultaneously. KRT16P2 inhibited miR-1294 expression, and miR-1294 inhibited EGFR expression through direct binding. miR-1294 overexpression repressed LSCC cell proliferation and aggressiveness. The effects of KRT16P2 silence on the expression of EGFR, LSCC cell proliferation, invasion, and migration, the protein levels of ki-67, PCNA, and cleaved-Caspase 3, as well as the phosphorylation of AKT, were all significantly reversed by miR-1294 inhibition. In conclusion, we demonstrated a lncRNA KRT16P2/miR-1294/EGFR axis that regulates LSCC cell proliferation, invasion, and migration. The clinical application of this axis needs further in vivo and clinical investigation.
机译:喉鳞状细胞癌(LSCC)是最常见的头部和颈部恶性肿瘤之一。鉴定LSCC的早期诊断和个性化疗法的有效标记和/或靶标仍然是一个相当大的挑战。本研究分析了在线数据,并将LNCRNA KRT16P2鉴定为LSCC中的显着上调的长非编码RNA(LNCRNA)。 KRT16P2 LSCC细胞敲低抑制癌细胞增殖,入侵和迁移。类似于KRT16P2,在LSCC中也显着上调EGFR表达。 KRT16P2和EGFR在LSCC组织样品中呈正相关。 EGFR敲低也显着抑制了LSCC细胞增殖和侵略性(入侵和迁移)。通过在线数据和在线工具,预测MIR-1294将同时针对KRT16P2和EGFR 3'UTR。 KRT16P2抑制miR-1294表达,MiR-1294通过直接结合抑制EGFR表达。 miR-1294过表达抑制LSCC细胞增殖和侵略性。 KRT16P2静音对EGFR,LSCC细胞增殖,侵袭和迁移的表达,KI-67,PCNA和切割 - 胱天蛋白酶3的蛋白质水平以及AKT的磷酸化,MIR显着逆转-1294抑制。总之,我们证明了一种LNCRNA KRT16P2 / miR-1294 / EGFR轴,用于调节LSCC细胞增殖,入侵和迁移。这种轴的临床应用进一步在体内进行了进一步的临床调查。

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