The study aimed at investigating the effects of miR-30a-5p on the biological functions of oral cancer cells and figuring out the potential mechanism. We first verified the low expression of miR-30a-5p and high expression of FAP (Homo sapiens fibroblast activation protein α) in oral cancerous tissues and their negative correlation. Then, the target relationship between miR-30a-5p and FAP was validated by dual luciferase reporter assay and biotin-coupled miRNA pulldown assay. After transfection in Tca-8113 cells and SCC-15 cells, MTT, colony formation, Transwell, and wound healing assays were performed to investigate how miR-30a-5p and FAP adjusted propagation, invasiveness, and migration, respectively. Mounting evidence supported that miR-30a-5p directly targetted FAP and suppressed its expression in oral cavity cancer cells (OSCCs). By suppressing FAP expression, miR-30a-5p significantly inhibited cell propagation, migration, and invasion. Therefore, miR-30a-5p might be a new therapeutic target for oral cancer treatment.

MicroRNAs (miRNAs) are a cluster of short non-coding RNAs playing critical roles in human cancers. miR-187 was recently found to be a novel cancer-related microRNA. However, the expression and function of miR-187 in cervical cancer have not been investigated. In this study, we found that miR-187 level was decreased in cervical cancer tissues and cell lines. Patients with low level of miR-187 had significantly decreased rate of overall survival (OS) and progression-free survival (DFS). miR-187 overexpression inhibited proliferation and promoted apoptosis of cervical cancer cells, whereas miR-187 knockdown promoted proliferation and inhibited apoptosis of cervical cancer cells. Forced expression of miR-187 inhibited the subcutaneous growth of cervical cancer cells in nude mice. Furthermore, FGF9 was found to be the downstream target of miR-187 in cervical cancer cells. Importantly, targeting FGF9 was required for miR-187 exerting its tumor suppressive roles in cervical cancer cells.

Introduction Cervical cancer is the second most common type of cancer and the third leading cause of cancer deaths in females in developing countries. Recent studies showed that long non-coding RNAs play a key role in human cancers. However, the molecular mechanisms underlying the initiation and progression of cervical cancer remained to be further explored. Material and methods In this study, we explored the differential expression of lncRNAs and mRNAs in cervical cancer progression by analyzing the public dataset GSE63514. Next, PPI and co-expression networks were constructed to reveal the potential roles of cervical cancer related mRNAs and lncRNAs. Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was performed to explore functions of differentially expressed genes (DEGs) in cervical cancer. Results In the present study, we observed that 3021 mRNAs were up-regulated and 1605 mRNAs were down-regulated in cervical cancer progression. Meanwhile, we for the first time found that 172 lncRNAs were up-regulated and 106 lncRNAs were down-regulated in cervical cancer progression. Co-expression network analysis showed that lncRNAs were widely co-expressed with cell cycle related genes in cervical cancer, implicating the important roles of these lncRNAs in cell proliferation regulation. Of note, we identified two hub lncRNA-mRNA networks involved in regulating various biological processes in cervical cancer progression. Conclusions Our results identified key mRNAs and lncRNAs in cervical cancer progression. This study will provide novel insights to explore the potential mechanisms underlying cervical cancer progression.

ObjectiveThe objective of this systematic review and meta-analysis was to determine the prognostic value of memory CD8(+) T cells in cancer patients with immunotherapy.MethodsEMBASE, MEDLINE (PubMed), and Web of Science databases were searched to identify suitabile articles published before March 2021. Risk of bias on the study level was assessed using the Cochrane Bias Risk Assessment Tool. The hazard ratios (HRs) and 95% confidence intervals (CIs) of pooled progression-free survival (PFS) and overall survival (OS) were calculated using RevMan 5.4 to evaluate the prognostic impact of memory CD8(+) T cells.ResultsIn total, nine studies were included in the final analysis. High levels of memory CD8(+) T cells were significantly closely correlated with better progression-free survival (PFS) and overall survival (OS) of cancer patients with immunotherapy (PFS, HR 0.64, 95% CI 0.53–0.78; OS, HR 0.37, 95% CI 0.21–0.65). Memory CD8(+) T cells still have significant prognostic value in cancer patients given immunotherapy alone after excluding of other interfering factors such as chemotherapy, radiotherapy, and targeted therapy (PFS, HR 0.65, 95% CI 0.48–0.89; OS, HR 0.23, 95% CI 0.13–0.42). However, high memory CD8(+) T cells levels did not correspond to a longer PFS or OS in cancer patients with non-immunotherapy (PFS, HR 1.05, 95% CI 0.63–1.73; OS, HR 1.29, 95% CI 0.48–3.48). Thus, memory CD8(+) T cells might be a promising predictor in cancer patients with immunotherapy.ConclusionsThe host’s overall immune status, and not only the tumor itself, should be considered to predict the efficacy of immunotherapy in cancer patients. This study is the first to show the significant prognostic value of memory CD8(+) T cells in immunotherapy of cancer patients through systematic review and meta-analysis. Thus, the detection of memory CD8(+) T cells has a considerable value in clinical practice in cancer patients with immunotherapy. Memory CD8(+) T cells may be promising immunotherapy targets.

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