Increased sensitivity of human colon cancer cells to DNA cross-linking agents after GRP78 up-regulation

Biochem Biophys Res Commun. 1999 Apr 13;257(2):361-8. doi: 10.1006/bbrc.1999.0472.

Abstract

We have shown earlier that pre-treatment of V79 Chinese hamster cells with 6-aminonicotinamide (6-AN) or 2-deoxyglucose (2-dG) results in over-expression of the Mr 78,000 glucose-regulated stress protein (GRP78) and the subsequent development of resistance to inhibitors of topoisomerase II. These phenomena also occur in V79-derived cell lines that are deficient in poly(ADP-ribose) (p(ADPR)) metabolism. In contrast, over-expression of GRP78 under the conditions outlined above is found to be associated with hypersensitivity to several clinically-relevant DNA cross-linking agents, namely, 1,3-bis (2-chloroethyl)-1-nitrosourea (BCNU), cisplatin, and melphalan. We have also previously shown that pre-treatment with 6-AN, an inhibitor of p(ADPR) metabolism, causes an increase in the life span in BCNU-treated mice bearing L1210 tumors. These observations prompted us to examine whether 6-AN pre-treatment can result in the over-expression of GRP78 in human colon cancer cell lines and, if so, whether this increase is associated with sensitization to DNA cross-linking agents outlined above. Following treatment of three colon cancer cell lines, HCT116, SW480, and VACO-8, for 48 h with 0.1 mM 6-AN, cytosolic GRP78 levels were elevated approximately 4.2 times, 8 times, and 2.5 times for each cell line respectively, as measured by Western immunoblotting. To determine sensitivity after GRP78 up-regulation, the cells were washed and grown for 412 h in growth medium devoid of 6-AN, before being treated with DNA cross-linking agents. The 412 h time period allowed p(ADPR) metabolism to return to normal while GRP78 levels remained elevated, thus allowing us to associate GRP78 over-expression with sensitivity to those agents. After treating cells for 1 h with BCNU, cisplatin, or melphalan, cell sensitivity was determined by clonogenic survival assay or a fluorescence-based cytotoxicity assay. Based on changes in IC50 values, 6-AN caused an increase in sensitivity for HCT116, SW480, and VACO-8 cells of 1.5, 2.3, and 1.0 times, respectively, for BCNU, 4.8, 3.8, and 2.6 for cisplatin, and 6.4, 3.7, and 2.2 times for melphalan. Thus, our results show that over-expression of GRP78 in human tumor cell lines is associated with increased sensitivity to clinically useful chemotherapy agents. This sensitization occurred in three different tumor cell lines, each bearing a separate genetic defect associated with altered sensitivity.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 6-Aminonicotinamide / pharmacology*
  • Blotting, Western
  • Carmustine / pharmacology
  • Carrier Proteins / genetics
  • Carrier Proteins / metabolism*
  • Cell Survival / drug effects
  • Cisplatin / pharmacology
  • Colonic Neoplasms / genetics*
  • Colonic Neoplasms / metabolism
  • Cross-Linking Reagents / pharmacology*
  • DNA Damage / drug effects*
  • Dose-Response Relationship, Drug
  • Drug Resistance, Neoplasm
  • Endoplasmic Reticulum Chaperone BiP
  • Heat-Shock Proteins*
  • Humans
  • Melphalan / pharmacology
  • Molecular Chaperones / genetics
  • Molecular Chaperones / metabolism*
  • NAD / analogs & derivatives
  • NAD / biosynthesis
  • NAD / metabolism
  • Poly Adenosine Diphosphate Ribose / metabolism
  • Time Factors
  • Tumor Cells, Cultured
  • Up-Regulation / drug effects*

Substances

  • Carrier Proteins
  • Cross-Linking Reagents
  • Endoplasmic Reticulum Chaperone BiP
  • HSPA5 protein, human
  • Heat-Shock Proteins
  • Hspa5 protein, mouse
  • Molecular Chaperones
  • NAD
  • Poly Adenosine Diphosphate Ribose
  • 6-Aminonicotinamide
  • Cisplatin
  • Melphalan
  • Carmustine