Cartilage oligomeric matrix protein affects the biological behavior of papillary thyroid carcinoma cells by activating the PI3K/AKT/Bcl-2 pathway.

Cartilage oligomeric matrix protein affects the biological behavior of papillary thyroid carcinoma cells by activating the PI3K/AKT/Bcl-2 pathway.
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软骨寡聚基质蛋白通过激活PI3K/AKT/Bcl-2通路影响甲状腺乳头状癌细胞的生物学行为

DOI:
10.7150/jca.49144
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发表时间:
2021
期刊:
影响因子:
3.9
通讯作者:
Qiao H
Qiao H
中科院分区:
医学3区
文献类型:
--
作者:
Zhang J;Wang H;Lv C;Han J;Hao M;Li J;Qiao H

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目的:探讨软骨寡聚基质蛋白(COMP)在甲状腺乳头状癌(PTC)中的作用。方法:应用组织芯片技术检测癌旁组织及癌旁正常组织中COMP的表达水平。培养人PTC细胞并用针对COMP的慢病毒短发夹RNA(COMP-shRNA)、阴性对照(NC)shRNA或模拟转染(对照)转导。本研究采用Cell Counting Kit-8,通过集落形成实验、创伤愈合实验、Transwell侵袭实验、流式细胞术,以及在mRNA和蛋白水平上检测凋亡相关蛋白的表达,探讨COMP对PTC细胞生物学行为的影响,并揭示参与这些过程的特异性信号通路。结果:COMP在PTC组织中的表达明显高于癌旁正常组织。在细胞水平,COMP促进细胞迁移,增加PTC细胞的侵袭力,抑制细胞凋亡。然而,仅在72小时内观察到细胞增殖的差异。同时,集落形成实验表明沉默COMP抑制PTC细胞的增殖。我们还发现COMP通过激活PI 3 K/AKT/Bcl-2通路来调节PTC细胞的行为。结论:COMP在PTC中上调,其增强癌细胞侵袭并抑制凋亡,有助于PTC的发生和进展。因此,COMP可能作为PTC的一个新的生物标志物。
Objective: To explore the effect of cartilage oligomeric matrix protein (COMP) on papillary thyroid carcinoma (PTC). Methods: COMP expression levels in PTC tissues and matched adjacent normal tissues were measured using tissue microarrays. Human PTC cells were cultured and transduced with lentiviral short hairpin RNA against COMP (COMP-shRNA), a negative control (NC) shRNA, or mock transfected (Control). We used the Cell Counting Kit-8, performed colony formation assays, wound healing assays, Transwell invasion assays, flow cytometry, and measured the expression of apoptosis-related proteins at the mRNA and protein levels to explore the effects of COMP on the biological behavior of PTC cells and to discover the specific signaling pathway involved in these processes. Results: COMP expression was significantly higher in PTC tissues than in adjacent normal tissues. At the cellular level, COMP promoted cell migration, increased the invasiveness of PTC cells, and inhibited apoptosis. However, differences in cell proliferation were only observed within 72 hours. At the same time, colony formation assays showed that silencing COMP inhibited the proliferation of PTC cells. We also found that COMP regulated the behavior of PTC cells by activating the PI3K/AKT/Bcl-2 pathway. Conclusions: COMP is upregulated in PTC, which enhances cancer cell invasion and inhibits apoptosis, contributing to the development and progression of PTC. Thus, COMP may serve as a new biomarker for PTC.
DOI: 10.1002/cncr.27591
发表时间: 2012-11-15
期刊: CANCER
影响因子: 6.2
作者:
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