LncRNA BRCAT54 is downregulated and inhibits cancer cell proliferation by downregulating miR‐130b‐3p through methylation in prostate cancer
BRCAT54 and miR‐130b‐3p are two recently characterized critical players in cancer biology, while their functions in prostate cancer (PC) are unknown. From preliminary sequencing analysis, we observed altered expression of BRCAT54 and miR‐130b‐3p in PC and an inverse correlation between them. This st...
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Veröffentlicht in: | Journal of biochemical and molecular toxicology 2024-01, Vol.38 (1), p.e23552-n/a |
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Sprache: | eng |
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Zusammenfassung: | BRCAT54 and miR‐130b‐3p are two recently characterized critical players in cancer biology, while their functions in prostate cancer (PC) are unknown. From preliminary sequencing analysis, we observed altered expression of BRCAT54 and miR‐130b‐3p in PC and an inverse correlation between them. This study was conducted to explore their involvement in PC. A total of 64 PC patients were enrolled to collect paired PC and nontumor tissues. The expression of BRCAT54 and miR‐130b‐3p were determined by RT‐qPCR. Overexpression of BRCAT54 and miR‐130b‐3p was achieved in PC cells to explore their roles in regulating the expression of each other. Methylation‐specific PCR (MSP) was conducted to explore the role of BRCAT54 in regulating promoter methylation of miR‐130b‐3p. BrdU assay was used to evaluate the role of BRCAT54 and miR‐130b‐3p in regulating PC cell proliferation. The results showed that PC tissues exhibited downregulation of BRCAT54 and upreglation of miR‐130b‐3p compared to that in nontumor tissues. They were inversely correlated across PC tissue samples. Overexpression of BRCAT54 decreased RNA accumulation of miR‐130b‐3p in PC cells. In addition, overexpression of BRCAT54 increased promoter methylation of miR‐130b‐3p. Moreover, BRCAT54 suppressed the role of miR‐130b‐3p in promoting PC cell proliferation. In conclusion, BRCAT54 is downregulated in PC and it may inhibit cancer cell proliferation by downregulating miR‐130b‐3p through methylation. |
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ISSN: | 1095-6670 1099-0461 |
DOI: | 10.1002/jbt.23552 |