Decreased PANK1 expression in kidney renal clear cell carcinoma: impact on cell apoptosis, invasion, migration, and epithelial-mesenchymal transition

  • 0Department of Urology, Lishui People's Hospital, Lishui, 323000, Zhejiang, China.

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Summary

This summary is machine-generated.

Pantothenate kinase 1 (PANK1) is down-regulated in kidney renal clear cell carcinoma (KIRC). Restoring PANK1 inhibits cancer cell invasion and promotes apoptosis, suggesting PANK1 as a potential therapeutic target for KIRC.

Area Of Science

  • Oncology
  • Molecular Biology
  • Biochemistry

Background

  • Kidney renal clear cell carcinoma (KIRC) is a significant health concern.
  • The molecular mechanisms underlying KIRC progression require further elucidation.

Purpose Of The Study

  • To investigate the expression and role of pantothenate kinase 1 (PANK1) in KIRC.
  • To analyze the correlation between PANK1 expression and KIRC clinicopathological features and prognosis.
  • To explore the functional impact of PANK1 on KIRC cell invasion, migration, and apoptosis.

Main Methods

  • Bioinformatic analysis using GEPIA, UALCAN, and LinkedOmics for PANK1 expression in KIRC.
  • In vitro experiments involving KIRC cell lines (Caki-1, 786-O) and noncancerous renal cells (HK-2, RPTEC).
  • PANK1 overexpression studies utilizing wound healing, Transwell assays, Annexin V-FITC/PI staining, qRT-PCR, and Western blotting.

Main Results

  • PANK1 expression was significantly down-regulated in KIRC tissues and cells compared to normal controls.
  • Down-regulated PANK1 correlated with unfavorable clinicopathological features and prognosis in KIRC.
  • PANK1 overexpression inhibited KIRC cell invasion and migration while promoting apoptosis, partly by modulating epithelial-mesenchymal transition (EMT)-related genes.

Conclusions

  • PANK1 down-regulation is a common event in KIRC and is associated with disease progression.
  • PANK1 plays a crucial role in suppressing KIRC cell invasion and promoting apoptosis.
  • PANK1 represents a potential therapeutic target for KIRC treatment.