KIFC3 promotes the progression of non-small cell lung cancer cells through the PI3K/Akt pathway.

IF 2.3 3区医学 Q3 ONCOLOGY Thoracic Cancer Pub Date : 2024-10-11 DOI:10.1111/1759-7714.15465

Yu Mu, Haoxiang Liu, Anni Luo, Qingxiang Zhang

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Abstract

Background: Kinesin family member C3 (KIFC3), as reported, plays important roles in several tumor types. Nevertheless, it is unknown whether KIFC3 has effects on non-small cell lung cancer (NSCLC) development.

Materials and methods: KIFC3 expression was detected by RT-PCR, and its correlation with prognosis was analyzed by GEPIA website. Small interfering RNA against KIFC3 were adopted for modulating KIFC3 expression in NSCLC cells. KIFC3 effects on NSCLC cell proliferation were determined using the MTT and clone formation assay. Matrigel invasion and wound healing assays were adopted for measuring the invasion and migration capability of NSCLC cells. Western blot was applied for measuring the levels of proteins associated with the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) pathway in NSCLC cells.

Results: KIFC3 was markedly increased in NSCLC samples and cells. KIFC3 knockdown suppressed the proliferation, invasion, and migration in NSCLC. Mechanically, KIFC3 silencing suppressed NSCLC progression through inhibiting the PI3K/Akt pathway.

Conclusions: KIFC3 lack suppressed the proliferation, invasion, and migration which works, at least partially, by the PI3K/Akt pathway. These findings suggest that targeting KIFC3 via the PI3K/Akt pathway may offer a novel therapeutic strategy for NSCLC.

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KIFC3 通过 PI3K/Akt 通路促进非小细胞肺癌细胞的进展。

背景：据报道，驱动蛋白家族成员 C3（KIFC3）在多种肿瘤类型中发挥着重要作用。然而，KIFC3是否对非小细胞肺癌（NSCLC）的发展有影响尚不清楚：通过 RT-PCR 检测 KIFC3 的表达，并通过 GEPIA 网站分析其与预后的相关性。采用针对 KIFC3 的小干扰 RNA 调节 KIFC3 在 NSCLC 细胞中的表达。采用 MTT 和克隆形成试验测定了 KIFC3 对 NSCLC 细胞增殖的影响。采用 Matrigel 侵袭和伤口愈合试验测定 NSCLC 细胞的侵袭和迁移能力。采用 Western 印迹法测定 NSCLC 细胞中磷脂酰肌醇-3-激酶/蛋白激酶 B（PI3K/Akt）通路相关蛋白的水平：结果：KIFC3在NSCLC样本和细胞中明显增加。结果：KIFC3在NSCLC样本和细胞中明显增加，敲除KIFC3可抑制NSCLC细胞的增殖、侵袭和迁移。从机理上讲，KIFC3沉默通过抑制PI3K/Akt通路抑制了NSCLC的进展：结论：KIFC3的缺乏抑制了NSCLC的增殖、侵袭和迁移，而这至少部分是通过PI3K/Akt途径起作用的。这些研究结果表明，通过PI3K/Akt途径靶向KIFC3可能为NSCLC提供一种新的治疗策略。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Thoracic Cancer ONCOLOGY-RESPIRATORY SYSTEM

CiteScore

5.20

自引率

3.40%

发文量

439

审稿时长

2 months

期刊介绍： Thoracic Cancer aims to facilitate international collaboration and exchange of comprehensive and cutting-edge information on basic, translational, and applied clinical research in lung cancer, esophageal cancer, mediastinal cancer, breast cancer and other thoracic malignancies. Prevention, treatment and research relevant to Asia-Pacific is a focus area, but submissions from all regions are welcomed. The editors encourage contributions relevant to prevention, general thoracic surgery, medical oncology, radiology, radiation medicine, pathology, basic cancer research, as well as epidemiological and translational studies in thoracic cancer. Thoracic Cancer is the official publication of the Chinese Society of Lung Cancer, International Chinese Society of Thoracic Surgery and is endorsed by the Korean Association for the Study of Lung Cancer and the Hong Kong Cancer Therapy Society. The Journal publishes a range of article types including: Editorials, Invited Reviews, Mini Reviews, Original Articles, Clinical Guidelines, Technological Notes, Imaging in thoracic cancer, Meeting Reports, Case Reports, Letters to the Editor, Commentaries, and Brief Reports.