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Downregulation of hepatic lipase is associated with decreased CD133 expression and clone formation in HepG2 cells

Xuehua Liu1, Junhua Zuo2, Yuan Fang1

  • 1Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, P.R. China.

International Journal of Molecular Medicine
|July 18, 2018
PubMed

Insights

Lipase C (LIPC) downregulation in HepG2 cells reduced cancer cell proliferation and chemoresistance. LIPC inhibition also decreased CD133 expression and affected cell adhesion molecule pathways, suggesting LIPC as a potential cancer therapeutic target.

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • Cancer drug resistance impedes chemotherapy efficacy, necessitating novel therapeutic strategies.
  • Lipase C (LIPC) has been implicated in promoting colorectal cancer liver metastasis.
  • Understanding LIPC's role in cancer progression and chemoresistance is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the effects of LIPC on colorectal cancer cell proliferation, clone formation, and chemoresistance.
  • To analyze the relationship between LIPC expression, CD133 biomarker, and chemotherapy response in HepG2 cells.
  • To explore molecular pathways influenced by LIPC, including cell adhesion molecules (CAMs).

Main Methods:

  • Lipase C (LIPC) activity and expression were quantified using RT-qPCR and Western blot in HepG2 cells.
  • LIPC was downregulated using short hairpin RNA (shRNA) in HepG2 cells; proliferation, colony formation, and chemoresistance (doxorubicin, 5-FU) were assessed.
  • Flow cytometry (FACS) analyzed CD133 expression, while cDNA microarray and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis identified affected molecular pathways.

Main Results:

  • HepG2 cells exhibited higher LIPC activity and expression compared to other colon cancer cell lines.
  • LIPC downregulation decreased CD133 expression, reduced cell proliferation and colony formation, and increased chemoresistance.
  • KEGG analysis revealed altered cell adhesion molecule (CAM) pathways, including CLDN10 and CLDN1, suggesting LIPC's role in tumor progression.

Conclusions:

  • Downregulation of LIPC in HepG2 cells correlates with reduced proliferation, colony formation, and increased chemoresistance.
  • LIPC inhibition impacts CD133 expression and influences CAM pathways, highlighting its multifaceted role in cancer.
  • Lipase C (LIPC) represents a potential therapeutic target for improving chemotherapeutic efficacy in colorectal cancer.

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