Introduction Cervical cancer (CC) is a major health threat to women worldwide. Long non-coding RNA (lncRNA) has been reported to play crucial roles in regulating carcinogenesis, including CC. Methods In this work, levels of lncRNA forkhead box P4 antisense RNA 1 (FOXP4-AS1) in CC cell lines and normal cell lines were analyzed with quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) method. Effects of FOXP4-AS1 on CC cellular behaviors including proliferation, migration, and invasion were explored. Bioinformatic prediction tools and luciferase activity reporter assay were conducted to explore the downstream molecules for FOXP4-AS1. Results We found FOXP4-AS1 expression was significantly higher in CC cell lines than in normal cell line. Functionally, force FOXP4-AS1 expression increased CC cell proliferation, migration, and invasion, while FOXP4-AS1 knockdown caused opposite effects. Mechanistically, we found FOXP4-AS1 acts as competing endogenous RNA (ceRNA) for microRNA-136-5p (miR-136-5p) to regulate chromobox 4 (CBX4) expression. Discussion These findings indicated FOXP4-AS1 plays an oncogenic role in CC, which may provide novel therapeutic biomarker against CC. © 2020 Zhao et al.Purpose This research aimed to explore the role of miR-221-5p on the sensitivity of gastric cancer cells to cisplatin, and the proliferation and invasion of gastric cancer cells by regulating DDR1. Patients and Methods Altogether 69 patients who treated with radical gastrectomy from January 2014 to January 2016 were collected. With the agree of the patients, 69 gastric carcinoma and 69 adjacent tissues were taken, respectively, during the operation, and gastric carcinoma and human gastric mucosa cells were purchased. RT-PCR was used for detection of the expression level of miR-221-5p and DDR1. Wound healing assay and CCK-8 assay were used for exploration of the cell migration and viability. Western blot and double luciferase reporter gene were performed to determine the target gene of miR-221-5p. Results It was showed that miR-221-5p expression was decreased in GC tissues and cell lines. The high expression of miR-221-5p reduced the resistance of GC cells to cisplatin and inhibited the proliferation and migration of gastric cancer cells. The high expression of miR-221-5p promoted the proliferation, invasion and migration of GC cells. In addition, we found that DDR1 was a direct target gene of miR-221-5p in GC cells. We found that DDR1 expression increased in gastric carcinoma. Moreover, there was a negative correlation of DDR1 with the expression level of miR-221-5p. The increase of miR-221-5p increased the chemosensitivity of GC cells to cisplatin, and inhibited the proliferation, invasion, migration and EMT of GC cells by targeting DDR1. Conclusion The above research indicated that miR-221-5p may be a target for enhancing cisplatin chemotherapy sensitivity in gastric cancer patients. © 2020 Jiang et al.Background Prostate cancer (PCa) is a common malignant tumor of the urinary system in males. LncRNA taurine-upregulated gene 1 (TUG1) has been verified to play a crucial role in progression and prognosis of PCa. However, the functional mechanism of TUG1 remains unclear with radiosensitivity of PCa. https://www.selleckchem.com/products/ionomycin.html Methods Quantitative real-time PCR (qRT-PCR) was conducted to measure the transcription levels of genes. 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis were employed to assess cell proliferation and apoptosis, respectively. Moreover, colony formation assay was used to measure colony survival. Western blot was performed to detect the relative proteins expression. The interaction among variables was predicted by online tool starbase, and then confirmed using the dual luciferase reporter assay. A xenograft mouse model was constructed to investigate the effect of TUG1 on tumor growth in vivo. Results The levels of lncRNA TUG1 and SMC1A were remarkably increased, while miR-139-5p was downregulated in PCa. Patients with high expression of TUG1 showed a lower survival rate and poor prognosis. Knockdown of TUG1 inhibited PCa cell proliferation and colony survival fraction, and promoted apoptosis. Downregulation of miR-139-5p reversed the effects of TUG1 deletion on proliferation, apoptosis and colony survival fraction in PCa cells treated with 4 Gy of X-ray radiation. Moreover, TUG1 sponged miR-139-5p to regulate SMC1A expression. SMC1A deletion blocked the effects of TUG1 on the progression of PCa cells treated with 4 Gy of X-ray radiation. The tumor volume and weight were illustriously reduced with radiation and TUG1 silencing in xenograft model. Conclusion Knockdown of lncRNA TUG1 enhanced radiosensitivity in PCa via the TUG1/miR-139-5p/SMC1A axis. It may become a promising target for PCa treatment. © 2020 Xiu et al.Pediatric Philadelphia chromosome-like (Ph-like) acute B-lymphoblastic leukemia (B-ALL), a high-risk subset of B-ALL characterized by a gene expression profile similar to that of Ph-positive ALL, has extremely poor outcome after a relapse following autologous chimeric antigen receptor (CAR)-T and haploidentical (haplo) hematopoietic stem cell transplantation(HSCT)therapy. with very limited treatment options. Donor-derived CAR T-cell therapy, the most vital advanced anticancer technology, may be a promising salvage strategy for patients with Ph-like B-ALL. Here, we presented a relapsed and refractory case of a child with Ph-like B-ALL after autologous anti-CD19 CAR T-cell therapy followed by haplo-HSCT. She successfully achieved the fourth complete remission (CR4) and maintained CR for five months after the sequential infusion of donor-derived anti-CD22 and anti-CD19 CAR T cells, with mild CRS side effects and no obvious graft-versus-host disease. A donor-derived anti-CD22 and -CD19 CAR T-cell therapy combined with a sequential infusion strategy may provide a promising alternative treatment strategy as effective and safe salvage therapy for children with recurrent and refractory Ph-like B-ALL after autologous CD19-directed CAR T-cell therapy followed by haplo-HSCT. © 2020 Hua et al.Purpose Long non-coding RNAs (lncRNAs) play critical regulatory roles in the tumorigenesis of GC. This study aimed to investigate the regulatory effect and mechanism of lncRNA-HCG18 on GC. Methods The expression of lncRNA-HCG18 was detected in GC tissues and cell lines by qRT-PCR. LncRNA-HCG18 was silenced in AGS and MGC803 cells by the transfection of lncRNA-HCG18 siRNA (si-HCG18). MTT, transwell and Annexin V-PI double staining assay were performed to assess the proliferation, migration, invasion and apoptosis of GC cells. The expression of PI3K/Akt pathway-, apoptosis-, and migration-related proteins were detected by Western blot. An activator of PI3K/Akt pathway 740 Y-P was used to activate the PI3K/Akt pathway in AGS cells. A human tumor xenograft model was established in mice to evaluate the effects of si-HCG18 in vivo. Results LncRNA-HCG18 was overexpressed in GC tissues and cells. Up-regulation of lncRNA-HCG18 was positively correlated with the stage of tumor node metastasis and invasion depth. Silencing of lncRNA-HCG18 suppressed the proliferation, migration and invasion, and induced the apoptosis of GC cells.