Johnsonmacleod1532

The bromodomain and extra‑terminal domain (BET) family proteins are essential epigenetic regulators in lung cancer. However, BET inhibitors have not had the anticipated therapeutic efficacy. Combined treatment using BET inhibitors along with other drugs had favorable therapeutic effects but the underlying molecular mechanisms remain elusive. The aim of the present study was to investigate the antineoplastic effects and mechanisms of a combination of a BET inhibitor and paclitaxel or cisplatin in non‑small cell lung cancer (NSCLC). By using the online Kaplan‑Meier plotter, it was revealed that increased mRNA levels of several BET protein‑coding genes were associated with poor prognosis in NSCLC. SRB assay results revealed that pharmaceutical or genetic targeting of BET proteins suppressed the growth of NSCLC cells. Inhibition of BET protein expression, in combination with the use of chemotherapeutic drugs such as paclitaxel and cisplatin, further restrained NSCLC cell growth in a synergistic manner. Mechanistically, this combination of suppression of BET expression and chemotherapeutic treatment blocked NSCLC cell growth by inhibiting autophagy and promoting apoptosis, which were revealed by both western blot and ELISA results. The present findings revealed a new rationale for using a combination of BET inhibitors with chemotherapy in NSCLC treatment.Circular RNAs (circRNAs) are a group of regulators that affect the aggressive behaviors of several types of cancer. Hsa_circ_0001666 (also referred to as hsa_circ_000742) is a newly discovered circRNA that is upregulated in human papillary thyroid carcinoma (PTC) based on microarray analysis. However, the role of hsa_circ_0001666 in PTC progression remains unknown. Thus, the aim of the present study was to determine the potential function and underlying mechanism of hsa_circ_0001666 in PTC. The results demonstrated that hsa_circ_0001666 was upregulated in both PTC clinical samples and cell lines. Its expression was associated with lymph node metastasis of patients with PTC. Knocking down hsa_circ_0001666 expression inhibited cell proliferation, as evidenced by decreased cell viability, arrest of cell cycle progression at the G1 phase and an increase in cell cycle‑associated proteins. Apoptosis rates and expression levels of pro‑apoptotic proteins were also increased by silencing hsa_circ_0001666. In xenograft experiments, the oncogenic effect of hsa_circ_0001666 on tumor growth was verified. Additionally, luciferase reporter assays showed that hsa_circ_0001666 and ETS variant transcription factor 4 (ETV4) shared common binding sites with three microRNAs [(miRNA/miR)‑330‑5p, miR‑193a‑5p and miR‑326]. Knockdown of these miRNAs separately reversed the inhibitory effect of hsa_circ_0001666 small interfering RNAs on PTC tumor aggressiveness, and ETV4 overexpression also induced a similar effect to that of miRNA inhibitors. Thus, hsa_circ_0001666 may function as an oncogene, promoting PTC tumorigenesis via the miR‑330‑5p/miR‑193a‑5p/miR‑326/ETV4 pathway. This provides a basis for identifying potential novel therapeutic targets for PTC.It has been reported that microRNAs (miRs) contribute to several biological functions and are associated with drug resistance in various types of cancer. However, to the best of our knowledge, whether miR‑613 can affect cisplatin (CDDP) sensitivity in non‑small cell lung cancer (NSCLC) remains unknown. Reverse transcription‑quantitative PCR was performed to detect the expression levels of miR‑613 and gap junction α‑1 protein (GJA1) in patients with NSCLC. Cell Counting Kit‑8, colony formation and Transwell assays were employed to exam the effects of miR‑613 and GJA1 on cell functions. Cell apoptosis was analyzed using flow cytometry. An in vivo experiment was conducted to determine the influence of miR‑613 on tumor formation. In the present study, miR‑613 was revealed to be significantly downregulated in lung cancer tissues compared with in adjacent normal tissues, and low miR‑613 expression indicated a poor prognosis. Furthermore, cell proliferation, colony formation and migration of lung cancer cells were inhibited by overexpression of miR‑613. In vivo experiments also demonstrated that miR‑613 could inhibit tumor growth. Moreover, miR‑613 could enhance the negative effects of CDDP on cell proliferation, apoptosis and migration. GJA1 was revealed to be a target gene of miR‑613 and was upregulated in human lung cancer tissues. Rescue experiments demonstrated that miR‑613 increased the chemosensitivity of lung cancer cells by targeting GJA1. Collectively, the results suggested a tumor suppressor role of miR‑613 in NSCLC and indicated that miR‑613 could strengthen CDDP sensitivity in NSCLC cells by targeting GJA1, which may provide a novel therapeutic target for NSCLC.High‑risk human papillomavirus (HPV)16 and 18 are the primary cause of cervical cancer (CC) and long non‑coding RNAs (lncRNAs/lncs) are often abnormally expressed in patients with CC. The authors' previous study indicated that oncogenic enhancer of zeste homolog 2 (EZH2)‑binding lncRNA in cervical cancer (lnc‑EBIC) serves a role in the tumorigenic activity of the HPV E6 protein in patients with CC. However, whether HPV E7 affects the development of CC through lnc‑EBIC, and the potential mechanisms underlying this remains unclear. Therefore, the present study investigated the effects of lnc‑EBIC and HPV E7 in cervical cancer cell lines HeLa, CaSki and C33A in vitro. CCK‑8, EdU and DAPI staining assays, flow cytometry, RT‑qPCR, western blotting and Transwell assay were performed on these cell lines. The results revealed that exogenous expression of HPV16/18 E7 significantly promoted lnc‑EBIC expression, and conversely, lnc‑EBIC was downregulated by silencing endogenous HPV16/18 E7 expression in corresponding Cacular mechanism and potential therapeutic target for CC.Tissue‑specific transplantation antigen P35B (TSTA3) expression is upregulated in esophageal squamous cell carcinoma and breast cancer, and functions as an oncogene in breast cancer. However, the roles and underlying mechanisms of TSTA3 in lung cancer have not been fully elucidated. The current study aimed to reveal the role of TSTA3 in lung cancer and explore whether TSTA3 may be modulated by microRNA (miR)‑125a‑5p to activate β‑catenin signaling. Immunohistochemical staining and western blotting were used to analyze TSTA3 expression in lung cancer tissues and cells. Cell functions were assessed via Cell Counting Kit‑8, flow cytometry, wound‑healing, Transwell and in vivo tumor formation assays. The effect of TSTA3 on the activation of β‑catenin signaling was determined using western blot and immunofluorescence analyses. The association between miR‑125a‑5p and TSTA3 was determined by western blotting and luciferase gene reporter assay. this website The present study revealed that, compared with normal tissues and cells, TSTA3 expression was significantly increased in lung cancer tissues and cell lines, and high TSTA3 expression predicted a poor prognosis and more malignant clinical features in patients with lung cancer.