Department of Colorectal and Anal Surgery, Binzhou Medical University Hospital, No. 661, Huanghe 2nd Road, Binzhou, Shandong, 256603, P.R. China.
Shandong University, No. 661, Cultural West Road, Jinan, Shandong, 250014, P.R. China.
J Cancer Res Clin Oncol. 2024 Aug 7;150(8):386. doi: 10.1007/s00432-024-05910-3.
Colorectal cancer (CRC) remains a highly prevalent gastrointestinal neoplasm, presenting significant prevalence and lethality rate. DEAD/H box RNA helicase 10 (DDX10) has been proposed as a potential oncogene in CRC, the specific action mechanism by which DDX10 modulates the aggressive biological cellular events in CRC remains implicitly elucidated, however. During this study, DDX10 expression was detected via RT-qPCR and Western blotting. Cell proliferation was estimated via EDU staining. TUNEL staining and Western blotting appraised cell apoptosis. Cell stemness was evaluated by sphere formation assay, RT-qPCR, Western blotting as well as immunofluorescence staining. Relevant assay kit examined aldehyde dehydrogenase (ALDH) activity. Western blotting and immunofluorescence staining also detected autophagy. DDX10 was hyper-expressed in CRC cells. Down-regulation of DDX10 hampered cell proliferation, aggravated the apoptosis while eliminated the ability to form spheroid cells in CRC. In addition, DDX10 deletion improved ATG10 expression and therefore activated autophagy in CRC cells. Consequently, ATG10 depletion or treatment with autophagy inhibitor 3-Methyladenine (3-MA) partially compensated the influences of DDX10 silencing on the proliferation, apoptosis and stemness of CRC cells. Accordingly, DDX10 deficiency may aggravate autophagy mediated by ATG10 to impede cell proliferation, stemness and facilitate cell apoptosis, hence blocking the progression of CRC.
结直肠癌（CRC）仍然是一种高发的胃肠道肿瘤，具有较高的发病率和致死率。DEAD/H 盒 RNA 解旋酶 10（DDX10）已被提出是 CRC 中的一个潜在癌基因，然而，DDX10 调节 CRC 中侵袭性生物学细胞事件的具体作用机制仍不明确。在本研究中，通过 RT-qPCR 和 Western blot 检测 DDX10 的表达。通过 EDU 染色评估细胞增殖。通过 TUNEL 染色和 Western blot 评估细胞凋亡。通过球体形成实验、RT-qPCR、Western blot 和免疫荧光染色评估细胞干性。通过相关检测试剂盒检测醛脱氢酶（ALDH）活性。Western blot 和免疫荧光染色也检测自噬。DDX10 在 CRC 细胞中高表达。DDX10 下调阻碍细胞增殖，加重细胞凋亡，消除 CRC 中形成球体细胞的能力。此外，DDX10 缺失可提高 ATG10 的表达，从而激活 CRC 细胞中的自噬。因此，ATG10 耗竭或自噬抑制剂 3-甲基腺嘌呤（3-MA）处理部分补偿了 DDX10 沉默对 CRC 细胞增殖、凋亡和干性的影响。因此，DDX10 缺失可能通过 ATG10 加剧自噬，从而阻碍细胞增殖、干性并促进细胞凋亡，从而阻止 CRC 的进展。
