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Overexpression of miR-138-5p suppressed GC cell proliferation, migration, increased cell apoptosis as well as inhibited the tumor growth in vivo. DEK oncogene was predicted as a potential target of miR-138-5p. MiR-138-5p bound the 3'-UTR of DEK and inhibited the level of DEK in GC cells. Restoration of DEK abrogated miR-138-5p overexpression-mediated suppression of GC cell proliferation and cell cycle arrest.<br /><br /> Our results demonstrated the anti-cancer role of miR-138-5p in GC by targeting DEK, which suggested miR-138-5p as a potential therapeutic target for the treatment of patient with GC.<br /><br />Our results demonstrated the anti-cancer role of miR-138-5p in GC by targeting DEK, which suggested miR-138-5p as a potential therapeutic target for the treatment of patient with GC.<br /><br /> Ovarian cancer is the leading cause of death in gynecologic malignancies. Growing evidences demonstrate that a complicated relationship exists between the gut microbiota and cancer treatment. However, there are few studies explored the alterations of gut microbiota in ovarian cancer patients following anti-cancer treatments. Therefore, we aim to analyze the changes of the gut microbiota in ovarian cancer patients treated with radical surgery and chemotherapy.<br /><br /> The microbial genes were examined from a total of 75 fecal samples from 18 ovarian cancer patients, including 10 preoperative fecal samples (Group B), 4 postoperative fecal samples (Group M0), as well as 61 fecal samples after first to fifth cycles of chemotherapy, using 16S rRNA sequencing.<br /><br /> Our results showed that fecal samples collected in postoperative (Group M0) exhibited significant decreases in abundance of Bacteroidetes and Firmicutes, while a significant increase in abundance of Proteobacteria compared with preoperative (Group B) fecal sampr.<br /><br /> This study aimed to investigate the role of lncRNA MCM3AP-AS1 in colorectal cancer (CRC).<br /><br /> Paired tumor and non-tumor tissues were collected from 60 CRC patients. Expression of MCM3AP-AS1 was determined by RT-qPCR. Overexpression of MCM3AP-AS1, miR-545, and CDK4 in CRC cells was achieved to explore the interactions between them. Cell cycle assay was performed to analyze the roles of MCM3AP-AS1, miR-545, and CDK4 in regulating the cell cycle progression of CRC cells.<br /><br /> We found that MCM3AP-AS1 was upregulated in CRC and its high expression levels predicted poor survival of CRC patients. MCM3AP-AS1 is predicted to interact with miR-545. In CRC cells, overexpression of MCM3AP-AS1 and miR-545 was achieved, while their overexpression did not affect the expression of each other. Instead, overexpression of MCM3AP-AS1 led to the increased expression levels of CDK4, which is a downstream target of miR-545. Cell cycle analysis showed that overexpression of MCM3AP-AS1 and CDK4 suppressed G1 arrest induced by miR-545. In addition, overexpression of MCM3AP-AS1 reduced the enhancing effects of overexpressing miR-545 on cell cycle progression.<br /><br /> MCM3AP-AS1 may upregulate CDK4 by sponging miR-545 to induce G1 arrest in CRC cells.<br /><br />MCM3AP-AS1 may upregulate CDK4 by sponging miR-545 to induce G1 arrest in CRC cells.[This retracts the article DOI 10.2147/CMAR.S211651.].Poly (ADP-ribose) polymerase inhibitors (PARPi) are a unique class of antineoplastic agents that function by inducing synthetic lethality. Synthetic lethality occurs when PARPi and either another agent or an underlying genetic alteration together lead to overwhelming DNA damage and ultimately cell death. PARPi first showed promise as a cancer therapy in patients with BRCA1/2 mutations and have become part of standard treatment for breast and ovarian cancer. In prostate cancer, two PARPi, rucaparib and olaparib, have been FDA approved for the treatment of metastatic castration-resistant prostate cancer (mCRPC). While both agents are approved for tumors with BRCA1/2 alterations, for olaparib the indication is also expanded to patients with 12 other homologous recombination deficiency (HRD) gene alterations including ATM and PALB2. PARPi differ in their pharmacokinetics and pharmacodynamics, and additional studies are being conducted with niraparib, veliparib, and talazoparib in prostate cancer. While PARPi are fairly well tolerated, common toxicities include hematologic (anemia/thrombocytopenia) and gastrointestinal effects (nausea/vomiting). [https://www.selleckchem.com/products/ox04528.html GPR agonist] Ongoing studies are being conducted combining PARPi with other agents in patients with and without HRD alterations. Early data are promising for the combination of PARPi with second-generation antiandrogens and with immunotherapy. As additional trials are developed and reported, the hope is that the patient population who may benefit from PARPi will continue to expand.<br /><br /> Many studies have confirmed that circular (circRNA) is involved in the development of gastric cancer (GC). However, the role of circFLNA in the progression of GC remains unclear.<br /><br /> Quantitative real-time PCR (qRT-PCR) was used to measure the relative expression of circFLNA, microRNA (miR)-646 and 6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 2 (PFKFB2). Cell counting kit 8 (CCK8) assay, transwell assay and flow cytometry were performed to determine the proliferation, migration, invasion and apoptosis of cells, respectively. GC tumor xenograft models were built to confirm the function of circFLNA silencing on GC tumor growth in vivo. Furthermore, the lactate production, glucose consumption, ATP level and glucose uptake were detected to assess the glycolysis of cells. Then, the interaction between miR-646 and circFLNA or PFKFB2 was confirmed using dual-luciferase reporter assay. RNA immunoprecipitation (RIP) assay was used to verify the interaction between miR-646 and circFLNA further. In addition, Western blot (WB) analysis was employed to detect the relative protein expression of PFKFB2.<br /><br /> Our results found that circFLNA was upregulated in GC tissues and cells. Silencing of circFLNA could suppress the proliferation, migration, invasion, glycolysis, and enhance the apoptosis of GC cells. Also, circFLNA knockdown reduced GC tumor volume and weight in vivo. Further experiments revealed that circFLNA could sponge miR-646, and miR-646 could target PFKFB2. The rescue experiments indicated that miR-646 inhibitor could reverse the suppressive effect of circFLNA silencing on GC progression, and PFKFB2 overexpression also could invert the inhibition effect of miR-646 on GC progression.<br /><br /> Our data concluded that circFLNA played a pro-cancer role in GC, which suggested that circFLNA might be a potential biomarker for GC treatment.<br /><br />Our data concluded that circFLNA played a pro-cancer role in GC, which suggested that circFLNA might be a potential biomarker for GC treatment.