The Rho kinase pathway has previously been reported to possess a close relationship with the growth, migration and invasion of lung cancer cells. However, the molecular mechanisms underlying the effects of this pathway on lung cancer cells are still elusive. The aim of the present study was to investigate the effects and underlying molecular mechanisms of Ras homolog family member A (RhoA) on the proliferation and apoptosis of SPCA1 lung carcinoma cells. Stable SPCA1 lung cancer cell lines, in which RhoA expression was silenced by small interfering RNA, were isolated following Geneticin screening. Inhibition of RhoA expression significantly decreased the proliferation of SPCA1 lung cancer cells, whereas apoptosis was significantly increased (P<0.01) as determined by the MTS tetrazolium assay and flow cytometry analysis, respectively. At the molecular level, knockdown of RhoA resulted in the significant activation of caspase-3 (P<0.01), and a significant reduction in the levels of phosphorylated signal transducer and activator of transcription (phospho-STAT3; P<0.01), as determined by western blotting. The results suggested that RhoA knockdown prevents cell proliferation and induces apoptosis in SPCA1 lung cancer cells. Furthermore, the underlying mechanisms responsible for these effects may include the activation of caspase-3 and the reduction of phospho-STAT3 levels.

Background Lung adenocarcinoma (LUAD) is currently the leading cause of cancer-related death worldwide. Long noncoding RNAs (lncRNAs) play key roles in tumor occurrence and development as crucial cancer regulators. The present study aimed to explore the molecular mechanism and regulatory network of Linc00511 in LUAD and to identify new potential therapeutic targets for LUAD. Methods Real-time quantitative polymerase chain reaction (RT–qPCR) was performed to determine the relative Linc00511 levels in LUAD tissues and cells. The proliferation, apoptosis, migration, and invasion abilities of LUAD cells were assessed by a Cell Counting Kit-8 (CCK-8) assay, a colony formation assay, flow cytometry, and a Transwell assay. Changes in hsa_miR-126-5p, hsa_miR-218-5p, and COL1A1 expression were analyzed using western blotting and RT–qPCR. Targeted binding between miR-126-5p/miR-218-5p and Linc00511 or COL1A1 was verified with a luciferase reporter system and confirmed by an RNA pulldown assay. The participation of the PI3K/AKT signaling pathway was confirmed via western blotting. Xenograft animal experiments were performed to detect the impact of Linc00511 on LUAD tumor growth in vivo. Results In the present work, we observed that Linc00511 was upregulated in LUAD tissues and cells. Loss/gain-of-function experiments indicated that knockdown of Linc00511 significantly inhibited LUAD cell proliferation, migration and invasion and promoted LUAD cell apoptosis, whereas overexpression of Linc00511 showed the opposite effects. In addition, we determined that Linc00511 promoted COL1A1-mediated cell proliferation and cell motility by sponging miR-126-5p and miR-218-5p. Moreover, Linc00511 activated the PI3K/AKT signaling pathway through upregulation of COL1A1. Finally, silencing of Linc00511 inhibited LUAD tumor growth in vivo. Conclusions Linc00511 acts as a competing endogenous RNA to regulate COL1A1 by targeting miR-126-5p and miR-218-5p, thereby promoting the proliferation and invasion of LUAD cells.

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