We tried to identify the function of LINC01614 in lung adenocarcinoma (LUAD) and reveal its underlying mechanisms. qRT‐PCR was applied to assess the expression of LINC016014 in LUAD tissues, noncancerous tissues and cells. Through colony formation assay, MTT assay and apoptosis analysis, we examined the variation of cell proliferation and apoptosis ability after silencing LINC01614. Moreover, the targeting interactions among LINC01614, miR‐217 and FOXP1 were validated via luciferase reporter assay, and then, we regulated the expression of miR‐217 and FOXP1 to ascertain their importance in cell proliferation and apoptosis. LINC01614 and FOXP1 were found to be up‐regulated in LUAD tumours and cells, whereas miR‐217 was down‐regulated. The experiment showed that target‐specific selectivity exists between LINC01614‐miR‐217 and miR‐217‐FOXP1 3′UTR. Furthermore, we disclosed that inhibition of LINC01614 could activate miR‐217, which subsequently restrained FOXP1. It was proved that LINC01614 promoted FOXP1 by inhibiting miR‐217, which ultimately stimulated the development of LUAD.

Increasing evidence demonstrates that long noncoding RNAs (lncRNAs) play critical roles in human breast cancer (BC) tumorigenesis. However, the mechanisms by which lncRNA and N6-methyladenosine (m6A) regulate BC tumorigenesis are still unclear. In the present research, LINC00958 was markedly overexpressed in BC tissue and cells, and LINC00958 upregulation promoted the tumor progression of BC cells. Mechanistically, m6A methyltransferase-like 3 (METTL3) gave rise to the upregulation of LINC00958 by promoting its RNA transcript stability. Moreover, LINC00958 acted as a competitive endogenous RNA for miR-378a-3p to promote YY1. Overall, these data provide novel insight into how m6A-mediated LINC00958 regulates BC tumorigenesis.

Long–non‐coding RNAs (lncRNA) AWPPH promotes the progression of liver and bladder cancer, indicating its oncogenic role. The current study aimed to explore the involvement of AWPPH in triple‐negative breast cancer (TNBC). In the current study, we found that plasma levels of lncRNA AWPPH and microRNA‐21 (miRNA‐21) were upregulated in patients with TNBC than in healthy controls, and the upregulation of plasma lncRNA AWPPH and miRNA‐21 distinguished early‐stage patients with TNBC from healthy controls. Plasma levels of lncRNA AWPPH and miRNA‐21 were significantly and positively correlated in both patients with TNBC and healthy controls. LncRNA AWPPH and miRNA‐21 overexpression led to promoted cancer cells proliferation and improved cancer cell viability under carboplatin treatment, while lncRNA AWPPH small interfering RNA (siRNA) silencing played an opposite role. In addition, miRNA‐21 overexpression attenuated the effects of lncRNA AWPPH siRNA silencing on of cancer cell behaviors. LncRNA AWPPH overexpression led to upregulated miRNA‐21 in TNBC cells, while miRNA‐21 overexpression also led to significantly upregulated lncRNA AWPPH expression. Therefore, lncRNA AWPPH and miRNA‐21 may regulate cancer cell proliferation and chemosensitivity in TNBC by interacting with each other.