RHBDD2 overexpression promotes a chemoresistant and invasive phenotype to rectal cancer tumors via modulating UPR and focal adhesion genes

Biochim Biophys Acta Mol Basis Dis. 2020 Aug 1;1866(8):165810. doi: 10.1016/j.bbadis.2020.165810. Epub 2020 Apr 25.

Abstract

The current standard of care for locally advanced rectal cancer (RC) is neoadjuvant radio-chemotherapy (NRC) with 5-fluorouracil (5Fu) as the main drug, followed by surgery and adjuvant chemotherapy. While a group of patients will achieve a pathological complete response, a significant percentage will not respond to the treatment. The Unfolding Protein Response (UPR) pathway is generally activated in tumors and results in resistance to radio-chemotherapy. We previously showed that RHBDD2 gene is overexpressed in the advanced stages of colorectal cancer (CRC) and that it could modulate the UPR pathway. Moreover, RHBDD2 expression is induced by 5Fu. In this study, we demonstrate that the overexpression of RHBDD2 in CACO2 cell line confers resistance to 5Fu, favors cell migration, adhesion and proliferation and has a profound impact on the expression of both, the UPR genes BiP, PERK and CHOP, and on the cell adhesion genes FAK and PXN. We also determined that RHBDD2 binds to BiP protein, the master UPR regulator. Finally, we confirmed that a high expression of RHBDD2 in RC tumors after NRC treatment is associated with the development of local or distant metastases. The collected evidence positions RHBDD2 as a promising prognostic biomarker to predict the response to neoadjuvant therapy in patients with RC.

Keywords: Focal adhesion; Neoadjuvancy; RHBDD2; Rectal cancer; UPR.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antimetabolites, Antineoplastic / pharmacology
  • Caco-2 Cells
  • Cell Adhesion / drug effects
  • Cell Movement / drug effects
  • Cell Proliferation / drug effects
  • Drug Resistance, Neoplasm / genetics*
  • Endoplasmic Reticulum Chaperone BiP
  • Fluorouracil / pharmacology
  • Focal Adhesion Kinase 1 / genetics
  • Focal Adhesion Kinase 1 / metabolism
  • Focal Adhesions / drug effects
  • Gene Expression Regulation, Neoplastic*
  • HCT116 Cells
  • Heat-Shock Proteins / genetics
  • Heat-Shock Proteins / metabolism
  • Humans
  • Lymphatic Metastasis
  • Membrane Proteins / genetics*
  • Membrane Proteins / metabolism
  • Neoadjuvant Therapy / methods
  • Paxillin / genetics
  • Paxillin / metabolism
  • Protein Binding
  • Rectal Neoplasms / genetics
  • Rectal Neoplasms / metabolism
  • Rectal Neoplasms / pathology
  • Rectal Neoplasms / therapy*
  • Signal Transduction
  • Transcription Factor CHOP / genetics
  • Transcription Factor CHOP / metabolism
  • Unfolded Protein Response / drug effects*
  • eIF-2 Kinase / genetics
  • eIF-2 Kinase / metabolism

Substances

  • Antimetabolites, Antineoplastic
  • DDIT3 protein, human
  • Endoplasmic Reticulum Chaperone BiP
  • Heat-Shock Proteins
  • Membrane Proteins
  • PXN protein, human
  • Paxillin
  • RHBDD2 protein, human
  • Transcription Factor CHOP
  • Focal Adhesion Kinase 1
  • PTK2 protein, human
  • EIF2AK3 protein, human
  • eIF-2 Kinase
  • Fluorouracil