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This study investigated the inhibitory effects of lncRNA HLA Complex Group 11 (HCG11) on non-small cell lung cancer (NSCLC) and the molecular mechanisms. Bioinformatics analysis was conducted to determine the downstream targeted gene miR-17-5p/p21 and predict their binding sites. qRT-PCR and Western blot were used to detect expression levels, and dual luciferase and RIP assays were adopted to verify binding relationship. The lncRNA HCG11/miR-17-5p/p21 axis was found to regulate drug resistance, proliferation, apoptosis, and cell cycle of A549 and A549-Gemcitabine (GEM) cells. HCG11 acted as a ceRNA binding to miR-17-5p, which repressed p21 expression in turn. In vivo experiments demonstrated that HCG11 hindered tumor growth. Therefore, lncRNA HCG11, by targeting the miR-17-5p/p21 axis, suppressed GEM resistance and malignant progression of NSCLC cells. This study provides a reference for investigating the potential value of lncRNA HCG11 in the diagnosis of NSCLC and finding potential targets against clinical chemotherapeutic resistance in NSCLC. [ABSTRACT FROM AUTHOR]

MALAT1 has been implicated in tumor progression. But the mechanism and role underlying MALAT1 in non-small cell lung cancer (NSCLC) cell resistance to gemcitabine (GEM) remain rarely understood. Through bioinformatics analysis, we predicted MALAT1/miR-27a-5p/PBOV1 regulatory axis and constructed GEM resistant A549/GEM cell line, and A549 was the parent cell line. qRT-PCR was utilized to assess MALAT1, miR-27a-5p and PBOV1 expression in A549 and A549/GEM cells. MTT method and colony formation assay were utilized to measure cell viability and cell proliferation. Flow cytometry was conducted to assess cell cycle and cell apoptosis. Wound healing and Transwell assays were conducted to measure cell migratory and invasive potentials. Dual-luciferase reporter gene assay and RNA immunoprecipitation were utilized to identify the targeted relationship between MALAT1 and miR-27a-5p, and the former assay was also utilized to determine the targeted relationship between miR-27a-5p and PBOV1. The impacts of MALAT1/miR-27a-5p/PBOV1 on tumor growth and GEM resistance of NSCLC cells in vivo were validated by using the tumor xenograft model. MALAT1 was observed to be highly expressed in tissues and cells of GEM resistant patients. Forced level of MALAT1 could markedly enhance A549 cell resistance to GEM, but this impact could be weakened by silencing MALAT1. MALAT1 downregulated miR-27a-5p level. PBOV1 was the target of miR-27a-5p and could significantly enhance GEM resistance of NSCLC cell. MALAT1 facilitated tumor growth in vivo via targeting miR-27a-5p/PBOV1 and enhanced resistance of NSCLC cells to GEM. MALAT1/miR-27a-5p/PBOV1 axis was implicated in NSCLC cell resistance to GEM. We deepened our understanding about how MALAT1 enhanced NSCLC cell resistance to GEM and provided development of therapeutic strategy for NSCLC with a possible target. • LncRNA MALAT1 was associated with gemcitabine resistance in NSCLC cells. • LncRNA MALAT1 targeted miR-27a-5p in NSCLC. • PBOV1 was the direct target of miR-27a-5p in NSCLC. • LncRNA MALAT1 enhanced non-small cell lung cancer cell resistance to gemcitabine by directly affecting miR-27a-5p/PBOV1 axis. [ABSTRACT FROM AUTHOR]

Lung cancer has a higher incidence and mortality rate than other cancers, and over 80% of lung cancer cases were classified as non-small-cell lung cancer (NSCLC). TRIM66 is one of the crucial members of TRIM, which has a deep connection with the behavior of various malignant tumors. But it remains uncertain regarding its exact function and underlying mechanism in NSCLC. In our study, qRT-PCR and Western blot were employed to validate that TRIM66 was overexpressed in NSCLC. The migration, invasion, and epithelial-mesenchymal transformation (EMT) progression of NSCLC cells were determined by Western blotting and Transwell experiments after knocking down TRIM66, and it was found that knockdown TRIM66 inhibited the migration, invasion, and EMT processes of NSCLC cells. Next, the binding relationship between TRIM66 and MMP9 was verified by Co-IP assay. After determining the interaction between them, rescue assays showed that overexpression of MMP9 was capable to promote the migration, invasion, and EMT of NSCLC cells. However, the transfection of si-TRIM66 could reverse this facilitating effectiveness. To sum up, we concluded that by targeting MMP9, TRIM66 could exert a cancer-promoting role in the progression of NSCLC cells. [ABSTRACT FROM AUTHOR]