Notes

A mixed methods look at the Paediatric Soft tissue Things (PMM) on the web collection.
Conclusion In summary, our results illustrated that HAND2-AS1 functions as miR-106a-5p sponge to regulate RBM24 expression, and to influence PCa progression.Background Circular RNA (circRNA) plays a critical role in tumorigenesis and tumor progression. Many studies indicate that circRNA Gprc5a is significantly upregulated and functions as an oncogene in a variety of cancers. However, the molecular mechanism of circGprc5a in liver cancer remains unclear. Methods qRT-PCR was used to measure the expression levels of circGprc5a, miR-1283, YAP1 and TEAD1 mRNA in hepatocellular carcinoma (HCC) tissues or cells. YAP1 and TEAD1 protein levels were detected by Western blot. CCK-8 assay, cell colony formation, BrdU incorporation and Annexin V-FITC/PI assays were performed to analyze the effects of circGprc5a and miR-1283 on cell proliferation and apoptosis. The relationship between circGprc5a, miR-1283, YAP1 and TEAD1 was analyzed using bioinformatic analysis and luciferase. The tumor changes in mice were detected by in vivo experiments. Results CircGprc5a was highly expressed in liver cancer, and closely related poor survival of patients with liver cancer. Knockout of circGprc5a inhibited proliferation of HCC and induced apoptosis. CircGprc5a activated the YAP1/TEAD1 signaling pathway by acting as a sponge for miR-1283. Furthermore, overexpression of miR-1283 abolished the promotion of circGprc5a on HCC cells. Therefore, miR-1283 expression correlated negatively with circGprc5a expression yet positively with the expression of YAP1/TEAD1 in liver cancer. Conclusion CircGprc5a promoted the development of HCC by inhibiting the expression of miR-1283 and activating the YAP1/TEAD1 signaling pathway.[This corrects the article DOI 10.2147/OTT.S231153.].Background Cervical cancer (CC) is a highly prevalent cancer and one of the main causes of death among women worldwide. The miR-181 family has turned out to be associated with tumorigenesis in a variety of tumors by regulating the expression of tumor-related genes. However, the mechanisms and biological function of miR-181c-5p in cervical squamous cell carcinoma (SCC) have not been well elucidated. Materials and methods SiHa cell lines with specific gene overexpression vectors were constructed. Targetscan was used to predict the binding site of miR-181c-5p and GSKIP. MTT assay was used to detect the clone formation rate. Flow cytometry was used to detect the apoptosis rate and to separate the cell markers. The Transwell test was used to detect cell invasion. Immunohistochemistry was used to detect protein expression in tumor tissues. Western Blotting was used to detect the expression levels of related proteins. Results GSKIP was predicted to be the target gene of miR-181c-5p in cervical SCC. MiR-181c-5p overexpression suppressed SiHa cells proliferation and promoted apoptosis; the protein expressions of Ki67 and PCNA were decreased, but the expressions of Caspase-3 and Bax/Bcl-2 were increased. The overexpression of miR-181c-5p inhibited the stem-like properties of SiHa cells; the expressions of SOX2, OCT4 and CD44 were decreased. Furthermore, miR-181c-5p upregulation limited the invasion of SiHa cells; the expression of E-cadherin was higher, but the expressions of N-cadherin and Vimentin were lower. MiR-181c-5p overexpression inhibited tumorigenesis in cervical SCC tissues; the expressions of Ki67, Caspase-3, CD44 and Vimentin in vivo were consistent with those in vitro. Conclusion Taken together, miR-181c-5p was able to mitigate the cancer cell characteristic and invasive properties of cervical SCC through targeting GSKIP gene.Objective miR-381 is implicated in the occurrence and development of various cancers, yet its role in head and neck squamous cell carcinoma (HNSCC) remains largely unknown. Pinometostat This study sought to research the direct target of miR-381 in HNSCC and investigate their roles in cancer progression. Methods miRNA and mRNA expression files of HNSCC were accessed from TCGA database and then processed for differential analysis. Bioinformatics databases were employed to predict the target mRNAs of the potential miRNA. qRT-PCR was conducted to determine the expression levels of the target miRNA and mRNA. Then, a series of in vitro experiments like CCK-8, colony formation assay, wound healing assay and transwell assay were performed to detect cell proliferation, migration and invasion. Dual-luciferase reporter gene assay was carried out for the further validation of the targeted relationship between the miRNA and mRNA. Results miR-381 was observed to be greatly down-regulated in HNSCC cells, and its overexpression could inhibit cell proliferation, migration and invasion. Besides, dual-luciferase reporter gene assay confirmed that STC2 was a direct target of miR-381, and their expression levels were reversely correlated. Moreover, rescue experiments demonstrated that overexpressing STC2 could rescue the inhibitory effect of miR-381 overexpression on cell proliferation, migration and invasion. Also, we verified that miR-381/STC2 exerted its function on HNSCC proliferation by mediating the FAK/PI3K/Akt/mTOR signaling pathway. Conclusion miR-381 suppresses cell proliferation, migration and invasion in HNSCC through targeting STC2, and participates in HNSCC development probably via the FAK/PI3K/Akt/mTOR signaling pathway.Vasculogenic mimicry (VM) is the formation of a "vessel-like" structure without endothelial cells. VM exists in vascular-dependent solid tumors and is a special blood supply source involved in the highly invasive tumor progression. VM is observed in a variety of human malignant tumors and is closely related to tumor proliferation, invasion, and recurrence. Here, we review the mechanism, related signaling pathways, and molecular regulation of VM in glioma and discuss current research problems and the potential future applications of VM in glioma treatment. This review may provide a new viewpoint for glioma therapy.As a result of the limited therapeutic options, advanced cervical cancer is difficult to treat, making the prognosis poor. Therefore, new therapeutic modalities or combinations need to be explored. We herein reported a case of stage IVB cervical cancer which was irresponsive to chemotherapy alone. Based on previous studies and after patient's consent was obtained, we made a therapeutic plan chemotherapy (albumin-bound paclitaxel and carboplatin) combined with immunotherapy (PD-1 inhibitor pembrolizumab). After 6 cycles of combined treatment, the patient got almost complete resolution with slight advent event. The treatment was further supported by local radiotherapy combined with immunotherapy. During the treatment period, disease was relatively stable, but the patient suffered severe grade 4 myelosuppression. We were therefore left with no other choice than to interrupt both chemotheraphy and radiotherapy. Before long, the tumor grew explosively again. These guided us to conclude that the combination use of albumin-bound paclitaxel (nab-paclitaxel) and carboplatin and pembrolizumab is effective and well tolerated in the treatment of advanced cervical cancer.
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