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KIFC3 通过 PI3K/Akt 通路促进非小细胞肺癌细胞的进展。

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

机构信息

School of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.

School of Traditional Chinese Medicine, Texas Health and Science University, Austin, Texas, USA.

出版信息

Thorac Cancer. 2024 Nov;15(33):2356-2364. doi: 10.1111/1759-7714.15465. Epub 2024 Oct 11.

DOI:10.1111/1759-7714.15465
PMID:39390964
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11586134/
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.

摘要

背景

驱动蛋白家族成员 C3(KIFC3)据报道在几种肿瘤类型中发挥重要作用。然而,目前尚不清楚 KIFC3 是否对非小细胞肺癌(NSCLC)的发展有影响。

材料与方法

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 来调节 NSCLC 细胞中的 KIFC3 表达。采用 MTT 和克隆形成实验来确定 KIFC3 对 NSCLC 细胞增殖的影响。采用 Matrigel 侵袭和划痕愈合实验来测量 NSCLC 细胞的侵袭和迁移能力。采用 Western blot 来检测 NSCLC 细胞中与磷脂酰肌醇-3-激酶/蛋白激酶 B(PI3K/Akt)通路相关的蛋白水平。

结果

KIFC3 在 NSCLC 样本和细胞中明显增加。KIFC3 敲低抑制了 NSCLC 的增殖、侵袭和迁移。在机制上,KIFC3 沉默通过抑制 PI3K/Akt 通路抑制 NSCLC 的进展。

结论

KIFC3 的缺失抑制了 NSCLC 的增殖、侵袭和迁移,至少部分是通过 PI3K/Akt 通路实现的。这些发现表明,通过 PI3K/Akt 通路靶向 KIFC3 可能为 NSCLC 提供一种新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/7368883cf7c1/TCA-15-2356-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/b9df019c167a/TCA-15-2356-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/8ee3593d3bf0/TCA-15-2356-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/880825d93d95/TCA-15-2356-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/7368883cf7c1/TCA-15-2356-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/b9df019c167a/TCA-15-2356-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/8ee3593d3bf0/TCA-15-2356-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/880825d93d95/TCA-15-2356-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/160b/11586134/7368883cf7c1/TCA-15-2356-g001.jpg

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