PRDM5 suppresses oesophageal squamous carcinoma cells and modulates 14–3‐3zeta/Akt signalling pathway

Nov 10, 2021Clinical and experimental pharmacology & physiology

PRDM5 slows esophageal cancer cells and influences a key cell survival pathway

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Circadian Biology on OpenScience ↗PubMed ↗DOI ↗

Abstract

PRDM5 expression in esophageal squamous cell carcinoma (ESCC) tissues is downregulated and correlates positively with overall survival.

Silencing PRDM5 expression increased cell proliferation in ESCC cells.
Overexpression of PRDM5 resulted in inhibited cell proliferation.
PRDM5 knockdown enhanced the migratory abilities of ESCC cells, while overexpression reduced migration.
PRDM5 negatively regulated the expression of 14-3-3zeta and the phosphorylation of Akt in ESCC cells.
In a tumor xenograft model, PRDM5 influenced ESCC tumor growth and the related protein expressions.

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Dysregulation of PR (PRDI-BF1 and RIZ) domain protein 5 (PRDM5) expression has been shown to be associated with the progression of many malignancies. Nevertheless, the role and underlying mechanism of PRDM5 in oesophageal squamous cell carcinoma (ESCC) remain elusive. qRT-PCR was performed to analyze PRDM5 mRNA expression, and western blot was used to determine protein expression of PRDM5, MMP-2, MMP-9, 14-3-3zeta, pan-Akt and phosphorylated Akt expression. CCK-8 staining was employed to evaluate cell proliferation, while wound scratch assay and Transwell assay were carried out to detect cell migration. A tumour xenograft model of ESCC was also established to validate the effect of PRDM5. PRDM5 expression was downregulated in ESCC tissues and positively correlated with the overall survival of ESCC patients. Silencing PRDM5 expression promoted cell proliferation in ESCC cells, while overexpressing PRDM5 inhibited cell proliferation. Moreover, the migratory abilities of ESCC cells were promoted by PRDM5 knockdown but were attenuated by PRDM5 overexpression. Importantly, 14-3-3zeta expression, along with the phosphorylation of Akt, was suppressed by PRDM5 in ESCC cells. In the established tumour xenograft model, PRDM5 regulated ESCC tumour growth as well as the expression of 14-3-3zeta and phosphorylation of Akt protein. In conclusion, PRDM5 suppresses ESCC cell proliferation and migration and negatively regulates 14-3-3zeta/Akt signalling pathway in vitro and in vivo.

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PRDM5 suppresses oesophageal squamous carcinoma cells and modulates 14–3‐3zeta/Akt signalling pathway

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