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.

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.

This study was to investigate the efficacy and safety of regorafenib or fruquintinib combined with camrelizumab in patients with microsatellite stable (MSS) and/or proficient mismatch repair (pMMR) metastatic colorectal cancer (mCRC).Medical records of MSS/pMMR mCRC patients who received regorafenib (80 mg) or fruquintinib (3 mg) once a day (21 days on/7 days off) plus camrelizumab (200 mg) every three weeks in Yuhuangding Hospital between January 2020 and June 2020 were retrospectively collected.Follow-up data up to November 1st, 2020 was gathered. The primary endpoint was the objective response rate (ORR) and disease control rate (DCR). The safety profile was the secondary endpoint.A total of 16 patients were enrolled. The ORR was 25.0% (4/16) and the DCR was 62.5% (10/16).The main adverse events (AEs) included reactive cutaneous capillary endothelial proliferation (RCCEP) (81.3%), fatigue (43.8%), hypertension (37.5%), hand-foot skin reaction (25.0%), and thyroid dysfunction (25.0%). Most AEs were grade 1 or 2, with only 1 patient of grade 3 liver dysfunction. All the AEs were ameliorated by effective symptomatic treatment.Regorafenib or fruquintinib plus camrelizumab exhibited promising efficacy in patients with MSS/pMMR mCRC. The toxicity was moderate and manageable.