Hsa-miR-1290 is associated with stemness and invasiveness in prostate cancer cell lines by targeting RORA.

This work examined microRNA-1290 (miR-1290)'s effect on regulating the malignant phenotype of prostate cancer (PC) cells. We detected miR-1290 expression within PC based on open-sourced datasets as well as in cancer cells and tissues. Loss-of-function experiments by miR-1290 knockdown in PC cell lines were performed. We performed CCK-8, clone forming, Transwell, and sphere formation assays for examining PC cells' malignant phenotypes following miR-1290 knockdown. We estimated miR-1290's target genes using online resources including miRDB, miRbase, miRTarBase and TargetScan. We also performed in vivo studies for validating how miR-1290 affected tumour formation within the mouse model. According to findings in this work, miR-1290 showed overexpression within PC cells and tissues. miR-1290 was indispensable for PC cell growth, stemness and invasion as well as mesenchymal status. Further, we identified RORA (retinoic acid receptor-related orphan receptor A) as miR-1290's target gene for mediating miR-1290 within PC cells. To sum up, this work suggests that miR-1290 up-regulation enhances PC cell growth and invasion by regulating RORA expression.

The antifibrotic effect of pheretima protein is mediated by the TGF-ß1/Smad2/3 pathway and attenuates inflammation in bleomycin-induced idiopathic pulmonary fibrosis.

ETHNOPHARMACOLOGICAL RELEVANCE: Pheretima is a traditional Chinese medicine that could treat various lung diseases such as asthma, pneumonia, and lung cancer effectively; however, limited studies on the use of Pheretima protein in the treatment of lung diseases have been conducted to date. AIM OF THE STUDY: The aim of this study was to explain the antipulmonary fibrosis mechanism of the Pheretima protein and elucidate its possible cell signaling pathways. MATERIAL AND METHODS: Fresh pheretima was freeze-dried to obtain the Pheretima protein. Divide C57BL/6 mice into control and bleomycin (BLM)-induced models, pirfenidone, and Pheretima protein-treatment groups. Three weeks later, they were treated with H&E and Masson's trichrome staining to assess lung injury and fibrosis. Pulmonary fibrosis was assessed using immunohistochemistry (IHC), realtime-PCR (RT-PCR), and western blotting. Inflammation was assessed using the alveolar lavage fluid. RESULTS: Pheretima protein inhibited epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) deposition and reduced inflammation. It also reduced the levels of Smad2/3, pSmad2/3, and transforming growth factor-beta 1 (TGF-ß1). Thus, our results indicate that Pheretima protein can alleviate BLM-induced pulmonary fibrosis in a mouse model. CONCLUSION: Pheretima protein inhibits ECM, EMT, and antiinflammatory markers, which in turn ameliorates BLM-induced pulmonary fibrosis. Preliminary mechanistic studies indicated that Pheretima protein can exert its biological activity by downregulating the TGF-ß1/Smad2/3 pathway.

High expression of citron kinase predicts poor prognosis of prostate cancer.

Citron kinase (CIT) is a Rho-effector protein kinase that is associated with several types of cancer. However, the role of CIT in prostate cancer (PCa) is unclear. The current study utilized microarray data obtained from The Cancer Genome Atlas, which was analyzed via Biometric Research Program array tools. Additionally, reverse transcription-quantitative (RT-q)PCR was performed to compare the mRNA expression of CIT in PCa tissue and in benign prostatic hyperplasia. The protein expression of CIT was detected in a consecutive cohort via immunochemistry and CIT was screened as a potential oncogene in PCa. The results of RT-qPCR demonstrated that the mRNA expression of CIT was increased in PCa tissues. Furthermore, immunochemistry revealed that CIT protein expression was positively associated with age at diagnosis, Gleason grade, serum PSA, clinical T stage, risk group, lymph node invasion and metastasis. When compared with the low expression group, patients with a high CIT expression exhibited shorter survival rates, cancer specific mortalities (CSM) and biochemical recurrence (BCR). In addition, multivariate analysis revealed that CIT was a potential predictor of CSM and BCR. The results revealed that CIT is overexpressed during the malignant progression of PCa and may be a predictor of a poor patient prognosis.

Rce1 expression in renal cell carcinoma and its regulatory effect on 786-O cell apoptosis through endoplasmic reticulum stress.

Ras and a-factor-converting enzyme 1 (Rce1) is located in the endoplasmic reticulum (ER) and is thought to be responsible for endoproteolytic processing of the vast majority of CAAX proteins. Endoplasmic reticulum stress (ERS) plays an important role in renal cell carcinoma (RCC); however, the expression and role of Rce1 in RCC have not been extensively studied. We aimed to investigate the expression of Rce1 in RCC tissues and its molecular mechanism in ERS-induced apoptosis in RCC 786-O cells. We first used western blotting, quantitative reverse transcriptase-polymerase chain reaction, and immunohistochemistry to detect the Rce1 expression in renal carcinoma tissues and paracancerous tissues. It was found that Rce1 expression was upregulated in RCC tissues, and its positive expression level was strongly associated with clinicopathologic features. Next, we detected the expression of Rce1 in human embryonic kidney cell line HEK293 and human renal carcinoma cell lines 786-O, ACHN, and A498. Higher expression of Rce1 was found in human renal carcinoma cell lines, especially in 786-O cells. Knockdown of Rce1 in 786-O cells increased apoptosis and inhibited proliferation (P < 0.05). Moreover, downregulation of Rce1 upregulated the expression of the pro-apoptotic protein Bax, but downregulated the expression of the anti-apoptotic protein Bcl-2. Further studies showed that downregulation of Rce1 also affected the expression of ERS factors. In conclusion, our results indicated that Rce1 plays a key role in RCC. Low expression of Rce1 might indirectly increase apoptosis and inhibit proliferation of renal carcinoma cells through ERS.