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Prostate cancer (PCa) is one of the most prevalent cancer types among males. Differential expression of microRNAs is associated with various cancers including PCa. Although mature microRNAs are preferentially located in the cytoplasm, several studies identified mature human microRNAs in purified nuclei and miR-145 has been found to be predominantly expressed in the nuclei of benign tissues compared to tumor lesions. However, the nuclear functions of miR-145 are yet limited. Here, we aimed at investigating the inductive role of miR-145 on the expression of Semaphorin 3A (SEMA3A) in PCa cell lines. To study the regulatory potential of miR-145 in the transcriptional level in PCa, we overexpressed miR-145 in PC3 and DU145 cells, and confirmed its upregulation by quantitative-real-time-PCR. Then we investigated the tumor suppressor potential of miR-145 upon inducing SEMA3A expression using cell viability assay, western blot analysis, Chromatin Immunoprecipitation assay and luciferase reporter assay. Our results revealed that p53, miR-145, and SEMA3A expressions are significantly downregulated in PC3 and DU145 cells compared to nontumorigenic prostate epithelial PNT1a cells. miR-145 overexpression in PCa cells induced the expression of SEMA3A at both messenger RNA and protein levels. Furthermore, increased miR-145 expression enriched RNA Pol-II antibody on the promoter of SEMA3A and induced luciferase activity controlled by SEMA3A promoter. In this study, we showed that the functions of miR-145 are not limited to gene silencing, and found that it may lead to changes in gene expression in the transcriptional level., (© 2021 International Federation for Cell Biology.)

Purpose: Peri-implantitis, a potentially progressive disease that occurs in patients with dental implants, is more aggressive than periodontal lesions, which makes the prevention of peri-implantitis an important priority. Due to problems in the early detection of peri-implantitis, there is an urgent need for discovering novel biologic molecules with the ability of early diagnosis. The goal of this study was to profile the microRNA content of saliva samples collected from patients with titanium-aluminum-vanadium alloy dental implants who experienced peri-implantitis and to find potential diagnostic markers for detection of this disease., Materials and Methods: The microRNA expression profiles of eight saliva samples (four collected from patients with peri-implantitis, four collected from patients who have successful implants) were investigated, and the deregulation of select microRNAs was further confirmed using quantitative polymerase chain reaction., Results: The expressions of 179 microRNAs were found as deregulated in the saliva of peri-implantitis patients in comparison to controls. Then, downregulation of miR-4484 was confirmed in the saliva of peri-implantitis patients in a larger validation cohort. Also, 40% of non-peri-implantitis patients and 78% of peri-implantitis patients had significantly decreased miR-4484 expression in saliva samples collected after 4 to 6 months subsequent to implant placement compared with samples collected before implant placement., Conclusion: Considering these findings, microRNA content of saliva might be proposed as a plausible source for the early diagnosis of peri-implantitis, where miR-4484 might serve as an encouraging early diagnostic biomarker.

Objectives: In this study, we aimed at investigating the expressions of miR-145 and its well-characterized direct targets on carboplatin treatment., Study Design: Laboratory study., Methods: The effect of carboplatin and miR-145 on the proliferative capacity of head and neck squamous cell carcinoma cells was evaluated using Cell Viability Detection Kit-8. Expressions of miR-145 and its targets were evaluated using quantitative real-time polymerase chain reaction on carboplatin treatment and p53 inhibition. Western blot was used to measure the levels of p53 and its acetylated versions in cells treated with carboplatin and/or pifithrin-α., Results: We demonstrated that carboplatin induced the expression of miR-145 in a dose-dependent manner and suppressed the expressions of miR-145 direct targets. In addition, we showed that inhibition of p53 by pifithrin-α in carboplatin-treated cells reduced miR-145 expression and reversed the suppression of miR-145 direct targets., Conclusions: Considering all these findings together, one of the proposed mechanisms of carboplatin to kill cells might be the induction of miR-145 and deregulation of its targets in parallel, via p53 activation, which happens through carboplatin's DNA-damaging property. To the best of our knowledge, these findings are the first to reveal the relationship between carboplatin and miR-145 in cancer cells., Level of Evidence: NA Laryngoscope, 2019., (© 2019 The American Laryngological, Rhinological and Otological Society, Inc.)