Psyllium extracts decreased neoplastic phenotypes induced by the Ha-Ras oncogene transfected into a rat liver oval

Yasushi Nakamura1, James E Trosko, Chia-Cheng Chang

  • 1Department of Pediatrics and Human Development, National Food Safety and Toxicology Bldg Center, Michigan State University, 243 Food Safety and Toxicology, East Lansing, MI 48824, USA.

Cancer Letters
|December 13, 2003
PubMed

Insights

Psyllium extract enhanced gap junctional intercellular communication (GJIC) and reduced anchorage-independent growth (AIG) in cancer cells. This suggests psyllium may reverse tumor-promoting effects of the Ha-ras oncogene.

Area of Science:

  • Oncology
  • Cell Biology
  • Carcinogenesis Research

Background:

  • Tumor promoters and oncogenes can inhibit gap junctional intercellular communication (GJIC), facilitating tumor progression by removing growth suppression from neighboring cells.
  • The WB-Ha-ras cell line exhibits deficient GJIC and anchorage-independent growth (AIG), key phenotypes associated with cancer development.

Purpose of the Study:

  • To investigate the effect of psyllium ethanol extract on GJIC and AIG in the WB-Ha-ras cell line.
  • To determine if psyllium can reverse oncogene-induced tumor cell phenotypes.

Main Methods:

  • Treatment of WB-Ha-ras cells with psyllium ethanol extract.
  • Quantification of GJIC using established assays.
  • Assessment of AIG by measuring colony number and size.
  • Histochemical staining for connexin43 to visualize gap junction protein expression.

Main Results:

  • Psyllium extract significantly increased GJIC by 1.65-fold in WB-Ha-ras cells.
  • Psyllium extract reduced both the number and size of colonies formed during anchorage-independent growth.
  • Histochemical analysis revealed that psyllium restored gap junction plaques (connexin43) on the plasma membrane.

Conclusions:

  • The ethanol extract of psyllium effectively reversed the GJIC deficiency and AIG phenotypes induced by the Ha-ras oncogene in WB-Ha-ras cells.
  • Psyllium demonstrates potential as an agent to counteract key cellular changes associated with tumor promotion and cancer progression.

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