Objective This study aimed to investigate the expression levels of miR‐133a‐3p and collagen type I α 1 (COL1A1) in esophageal squamous cell carcinoma (ESCC) to find out the relationship between miR‐133a‐3p and COL1A1 and their influence on ESCC propagation, migration, invasion, and apoptosis. Methods The messenger RNA expression levels of miR‐133a‐3p and COL1A1 in ESCC were detected by quantitative reverse‐transcription polymerase chain reaction. The expression of COL1A1 protein was examined via western blot analysis and immunohistochemistry assay. Cell propagation and apoptosis were, respectively, confirmed by CCK‐8 and flow cytometry assay, whereas cell mobility and invasiveness were analyzed by wound healing assay and transwell assay. The targeted relationship between miR‐133a‐3p and COL1A1 was validated by the dual luciferase reporter assay. The tumor xenograft model was constructed to further verify the impact of miR‐133a‐3p on esophageal squamous tumor growth and COL1A1 expression in vivo. Results miR‐133a‐3p was found low‐expressed whereas COL1A1 was highly expressed in esophageal squamous cancer tissue and cells. The expression of miR‐133a‐3p was negatively correlated with COL1A1 expression. The dual luciferase reporter gene assay confirmed that miR‐133a‐3p directly targeted COL1A1 and suppressed its expression. Cell Counting Kit‐8 assay, transwell assay, and flow cytometry analysis demonstrated that COL1A1 promoted ESCC propagation and invasion and suppressed cell apoptosis, whereas miR‐133a‐3p reversed such adverse effects by regulating COL1A1. Conclusions miR‐133a‐3p inhibited the cell propagation, invasion, and migration and facilitated apoptosis in ESCC by targeting COL1A1.

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Background: Thyroid cancer (TC) is an endocrine disease, and its progression is regulated by many factors, including circular RNAs (circRNAs). However, as a new circRNA, the role of circ_0058124 in TC is worth further exploration. Methods: The expression levels of circ_0058124, microRNA-940 (miR-940) and mitogen-activated protein kinase 1 (MAPK1) were assessed by quantitative polymerase chain reaction (q-PCR). The circular characteristic of circ_0058124 was identified by oligo (dT) 18 primers, Ribonuclease R (RNase R) and Actinomycin D (ActD), and its localization was determined by nuclear-cytoplasmic separation assay. Also, cell proliferation was detected by colony formation assay, and cell migration and invasion were assessed by transwell assay. Further, Seahorse XF Extracellular Flux Analyzer was used to measure the oxygen consumption rate (OCR) of cells. Besides, dual-luciferase reporter, RNA immunoprecipitation (RIP) and RNA pull-down assays were used to identify the mechanism of circ_0058124. Western blot (WB) analysis was used to test the MAPK1 protein level. In addition, mice xenograft models were constructed to test the effect of circ_0058124 on TC tumor growth in vivo. Results: Circ_0058124 was highly expressed in TC and is a stable cyclic transcript, mainly located in the cytoplasm. Circ_0058124 knockdown suppressed proliferation, migration, invasion and metabolic abilities in TC cells. MiR-940 could be absorbed by circ_0058124, and the inhibition effect of its overexpression on TC progression could be reversed by overexpressed-circ_0058124. MAPK1 was a target of miR-940, and the suppression effect of its silencing on TC progression could be inverted by miR-940 inhibitor. Besides, MAPK1 expression was regulated by circ_0058124 and miR-940. Interference of circ_0058124 also reduced TC tumor growth in vivo. Conclusion: Circ_0058124 might play a carcinogenic role in TC progression by regulating the miR-940/MAPK1 axis, which might provide a new idea for the treatment of TC.

Background Prostate cancer (PCa) is a leading cause of cancer-related death in males. Aberrant expression of long non-coding RNAs (lncRNAs) has been implicated in various human malignancies, including PCa. This study aims to clarify the inhibitory role of human PGM5 antisense RNA 1 (PGM5-AS1) in the proliferation and apoptosis of PCa cells. Methods The regulatory network of PGM5-AS1/microRNA-587 (miR-587)/growth and differentiation factor 10 (GDF10) axis was examined by dual-luciferase reporter gene assay, RNA-binding protein immunoprecipitation, and RNA pull down assay. We manipulated the expression of PGM5-AS1, miR-587 and GDF10 by transducing expression vectors, mimic, inhibitor, or short hairpin RNA into PCa cells, thus establishing their functions in cell proliferation and apoptosis. Additionally, we measured the tumorigenicity of PCa cells xenografted in nude mice. Results PGM5-AS1 is expressed at low levels in PCa cell lines. Forced overexpression of PGM5-AS1 restricted proliferation and facilitated apoptosis of PCa cells, manifesting in suppressed xenograft tumor growth in nude mice. Notably, PGM5-AS1 competitively bound to miR-587, which directly targets GDF10. We further validated that the anti-cancer role of PGM5-AS1 in PCa cells was achieved by binding to miR-587 to promote the expression of GDF10. Conclusion PGM5-AS1 upregulates GDF10 gene expression by competitively binding to miR-587, thus inhibiting proliferation and accelerating apoptosis of PCa cells.

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