Activity

If successful, this may move immune checkpoint inhibitors into the treatment armamentarium of prostate cancer management.Background Circular RNAs (circRNAs) have recently been reported to play essential roles in the progression of various cancers, including colorectal cancer (CRC). However, the roles of circRNA amyloid precursor-like protein 2 (circAPLP2) in CRC and its underlying mechanism have not been investigated. Materials and Methods The expression levels of circAPLP2, microRNA-485-5p (miR-485-5p), and forkhead-box K1 (FOXK1) were determined by quantitative real-time polymerase chain reaction. Cell proliferation, apoptosis, migration, and invasion were assessed by methylthiazolyldiphenyl-tetrazolium bromide assay, flow cytometry, and transwell assay, respectively. Western blot assay was performed to measure the protein levels of proliferating cell nuclear antigen, Bcl-2, Bax, vimentin, E-cadherin, fibronectin, and FOXK1. The interaction between miR-485-5p and circAPLP2 or FOXK1 was predicted by starBase and verified by dual-luciferase reporter assay. A xenograft tumor model was established to confirm the functions of circAPLP2 in vivo. The lactate production was measured using lactate assay kit. Results circAPLP2 expression was enhanced in CRC tissues and cells. circAPLP2 knockdown or miR-485-5p overexpression suppressed cell proliferation, migration, and invasion, whereas it promoted apoptosis in CRC cells, which was reversed by upregulating FOXK1. Moreover, miR-485-5p could directly bind to circAPLP2 and its downregulation reversed the suppressive effect of circAPLP2 knockdown on progression of CRC cells. In addition, FOXK1 was a downstream target of miR-485-5p. Furthermore, circAPLP2 modulated FOXK1 expression by sponging miR-485-5p in CRC cells. Besides, interference of circAPLP2 suppressed tumor growth in vivo and inhibited glycolysis in vitro by upregulating miR-485-5p and downregulating FOXK1. Conclusions circAPLP2 knockdown inhibited CRC progression through regulating miR-485-5p/FOXK1 axis, providing a novel avenue for treatment of CRC.Objective To explore clinical effects of neoadjuvant chemotherapy (NAC) in treating breast cancer. Materials and Methods Retrospective analysis was performed among 26 breast cancer patients receiving NAC. Chemotherapeutic effects were evaluated using Response Evaluation Criteria In Solid Tumors (RECIST), Japanese Breast Cancer Society (JBCS) grading, and Miller and Payne (MP) grading. Results After chemotherapy, the percentage of tumor cells was significantly reduced, but chemotherapeutic period possessed no dramatic influence on curative effects. Perifosine Among 20 patients with complete data, 2 achieved clinically complete response (CR), 10 showed partial response (PR), 4 had stable disease (SD), and 4 exhibited progress disease (PD). The total effective rate (CR + PR) of NAC was 60% (12/20). Besides, evaluation results from RECIST were generally in line with those from JBCS grading and MP grading. Conclusion NAC is effective among the majority of patients with breast cancer. In addition, tumor size determined through clinical palpation is generally in accordance with responses to chemotherapy, and consistent performance is observed for three systems in grading responses to chemotherapy.Background The incidence of thyroid cancer has increased dramatically in recent decades due, in large part, to identifications of subclinical diseases. Literature on thyroid cancer has examined the pathogenesis of high invasive papillary thyroid cancer (PTC) and has improved the prevention and treatment of PTC. This study aims to investigate the effects of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on PTC migration and invasion, and clarify the regulatory mechanisms between miR-146b-5p and MALAT1. Materials and Methods In this study, we examined the differential expression of MALAT1, miR-146b-5p, and DNA methyltransferases 3A (DNMT3A) in PTC tissues. The effect of MALAT1 on the proliferation and invasion ability of PTC cells was verified by constructing a sh-MALAT1 knockdown cell model. Correlations between MALAT1, miR-146b-5p, and DNMT3A were analyzed by the Pearson correlation method. Finally, we verified the regulatory relationship between miR-146b-5p and MALAT1 by the luciferase assay and rescue assay. Results The expression of MALAT1 was upregulated in PTC tissues and cells, while a MALAT1 knockdown counteracted cellular activity, migration, and invasion of B-CPAP and K1 cells. The relationship between miR-146b-5p and DNMT3A was negative, while the relationship between miR-146b-5p and MALAT1 was positive. Both genes were separately detected using the Pearson correlation method. The luciferase assay and rescue assay demonstrated that a binding site in miR-146b-5p was existent in the 3′ untranslated region of DNMT3A, while a knockdown of DNMT3A partially rescued si-miR-146b-5p induced proliferation, migration, and invasion effects on PTC cells. Conclusions The MALAT1 gene is highly expressed in PTC, while the knockdown MALAT1 gene attenuates the cellular activity and invasive ability of PTC cells. The microRNA miR-146b-5p can promote a MALAT1 expression by negatively regulating DNMT3A in PTC.BACKGROUND Patients often have quadriceps or hamstring weakness after anterior cruciate ligament reconstruction (ACLR), despite postoperative physical therapy regimens; however, little evidence exists connecting nerve blocks and ACLR outcomes. PURPOSE To compare muscle strength at return to play in patients who received a nerve block with ACLR and determine whether a specific block type affected subjective knee function. STUDY DESIGN Cohort study; Level of evidence, 3. METHODS Patients were recruited 5 to 7 months after primary, isolated ACLR and completed bilateral isokinetic strength tests of the knee extensor/flexor groups as a single-session return-to-sport test. Subjective outcomes were assessed with the International Knee Documentation Committee (IKDC) score. Strength was expressed as torque normalized to mass (N·m/kg) and limb symmetry index as involved/uninvolved torque. Chart review was used to determine the type of nerve block and graft used. Nerve block types were classified as knee extensor motor (femoral nerve), knee flexor motor (sciatic nerve), or isolated sensory (adductor canal block/saphenous nerve).