Lifestyle and Environment · Environmental Exposures

Gene expression changes in human lung cells exposed to arsenic, chromium, nickel or vanadium indicate the first steps in cancer

Clancy HA, Sun H, Passantino L, Kluz T, Muñoz A, Zavadil J, Costa M

Published August 2012 Metallomics : integrated biometal science
DOI 10.1039/c2mt20074k PMID 22714537 PMC PMC3563094

RRM Academy Synopsis

Four metals leave distinct lasting gene changes in cultured lung cells

A 2012 laboratory study of human airway cells reports that each of four metals left its own lasting pattern of cancer-related gene changes. Exposure to arsenic, chromium, nickel or vanadium produced 25 transformed clones, set against 11 control clones. The gene changes persisted through numerous cell divisions after the metal was removed.

Study at a glance, laboratory study of 25 transformed clones: Four metals left distinct lasting gene changes in lung cells
Study at a glance, laboratory study of 25 transformed clones: Four metals left distinct lasting gene changes in lung cells. Source: Clancy HA et al., 2012, PMID 22714537.

Key Findings

  • Researchers profiled 36 clones: 11 controls and 25 metal-transformed clones, of which 7 came from arsenic, 7 from nickel, 6 from chromium and 5 from vanadium, alongside 3 parental cell populations.
  • All 36 clones grouped by exposure in a principal component analysis. The control clones sat close to the parental cell lines.
  • A set of 4,231 genes showed significant increases or decreases in activity across several clones, for at least one metal among the four tested.
  • SATB2, a gene that modifies transcription, was up-regulated after all four metal treatments. Few genes changed consistently across every metal.
  • Clones from metal-treated cells could form tumors in nude mice. The control clones did not grow as xenografts.

Interpretation

The work is a laboratory study in BEAS-2B cells, a human lung-lining cell line grown in culture and exposed to each metal for 30 to 60 days. Its findings describe gene activity in those cultured cells. The authors hypothesize that the lasting changes come from altered epigenetic programs, meaning inherited controls on gene activity. They state that which changes drive cancer, and which are bystanders, is not known at this time. Because each metal produced its own pattern, the authors suggest the genes could serve as markers of early exposure.

RRM Context

Restorative reproductive medicine takes a root-cause view of health that includes a person's environment. The authors note that people meet arsenic, chromium and nickel worldwide at work and through pollution. They study the earliest cell changes because the authors consider prevention difficult without that knowledge.

Abstract

The complex process of carcinogenesis begins with transformation of a single cell to favor aberrant traits such as loss of contact inhibition and unregulated proliferation - features found in every cancer. Despite cancer's widespread prevalence, the early events that initiate cancer remain elusive, and without knowledge of these events cancer prevention is difficult. Here we show that exposure to As, Cr, Ni, or vanadium (V) promotes changes in gene expression that occur in conjunction with aberrant growth. We exposed immortalized human bronchial epithelial cells to one of four metals/metalloid for four to eight weeks and selected transformed clonal populations based upon anchorage independent growth of single cells in soft agar. We detected a metal-specific footprint of cancer-related gene expression that was consistent across multiple transformed clones. These gene expression changes persisted in the absence of the progenitor metal for numerous cell divisions. Our results show that even a brief exposure to a carcinogenic metal may cause many changes in gene expression in the exposed cells, and that from these many changes, the specific change(s) that each metal causes that initiate cancer likely arise.

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Lifestyle and Environment › Environmental Exposures › Heavy Metals
Hailey A Clancy, Hong Sun, Lisa Passantino, Thomas Kluz, Alexandra Muñoz, Jiri Zavadil, Max Costa
H Clancy, H Sun, L Passantino, Tom Kluz, T Kluz, Alex Muñoz, A Muñoz, J Zavadil, M Costa
PMID 22714537 22714537 DOI 10.1039/c2mt20074k 10.1039/c2mt20074k Clancy et al. 2012, Clancy 2012