miR-30d is related to asbestos exposure and inhibits migration and invasion in NCI-H2452 cells

Our plain-English summary of miR-30d is related to asbestos exposure and inhibits migration and invasion in NCI-H2452 cells, by L. Ju, W. Wu, X. Yin, et al (FEBS Open Bio, 2017).

The study

• Authors: L. Ju, W. Wu, X. Yin, Y. Xiao, Z. Jia, J. Lou, M. Yu, S. Ying, T. Chen, Z. Jiang, W. Li, J. Chen, X. Zhang, L. Zhu
• Journal: FEBS Open Bio
• Published: 2017;7(10):1469-1479
• Cited by: 6 articles, as counted by NIH iCite
• Read it: PubMed · Publisher · Free full text

Abstract

Pleural malignant mesothelioma (MM) is a highly aggressive tumor that is typically related to asbestos exposure and has a latency of 20-60 years. Several microRNA contribute to MM initiation and progression, but the mechanisms are not clear. Here, we found that miR-30d is downregulated in the pleural MM cell line NCI-H2452, in the plasma of asbestos-exposed individuals, and in asbestos-exposed mesothelial cells. Furthermore, we investigated the influence of the overexpression of miR-30d in pleural MM cells. We demonstrated that miR-30d overexpression could suppress pleural MM cell proliferation, migration, and invasion in vitro and could promote cell apoptosis but could not significantly influence cell cycle. The mRNA and protein expression of vimentin and TWIST1 decreased, and the mRNA expression of CDH1 increased in NCI-H2452 cells that overexpressed miR-30d. We therefore conclude that miR-30d is related to asbestos exposure and inhibits cell migration and invasion by regulating the epithelial-mesenchymal transition in NCI-H2452 cells.

In plain English

This laboratory study, with a small comparison of human blood samples, examined miR-30d, a small RNA molecule, in relation to asbestos and pleural malignant mesothelioma. In a pleural mesothelioma cell line (NCI-H2452), miR-30d levels were 0.671 times those in a normal mesothelial cell line (MeT-5A). In blood plasma, levels in 78 people from the Cixi area of Zhejiang, China, with more than 10 years of asbestos exposure were 0.766 times those in 39 unexposed people. Normal mesothelial cells treated with chrysotile had lower relative miR-30d levels (0.484 to 0.808) at times from 24 hours to 32 weeks. When the authors raised miR-30d levels in the mesothelioma cells, growth, migration and invasion fell and cell death (apoptosis) rose. The cell cycle did not change significantly. Gene activity of vimentin and TWIST1 fell. The authors concluded that miR-30d is related to asbestos exposure and inhibits migration and invasion in these cells. They noted that the unexposed group may have had environmental exposure, that the groups overlapped, and that more subjects are needed.

We wrote this plain-English summary from the full article with the help of AI, and a second AI model checked each sentence against the article. It is not the authors' wording; the abstract and the article are their own account.

What the study did and found

• Design: Laboratory (in vitro) cell-culture experiments, plus a comparison of plasma miR-30d levels between asbestos-exposed and unexposed people
• Who was studied: Two purchased human cell lines: NCI-H2452 (pleural malignant mesothelioma) and MeT-5A (normal pleural mesothelial cells). Also 117 residents of the Cixi area, Zhejiang Province, China, where asbestos product manufacturing started in the 1950s: 78 with more than 10 years of asbestos exposure and 39 unexposed. Both groups had a mean age of 68.22 years, and most participants were women. Dates of recruitment are not given.
• Exposure: Cell experiments used UICC standard chrysotile. MeT-5A cells were exposed at 0 to 80 micrograms per square centimetre for 24 hours to test toxicity, and at 5 micrograms per square centimetre for 24 hours up to 32 weeks (repeated weekly in long-term exposure). The exposed people were household hand-spinning women workers and workers in asbestos factories, with more than 10 years of exposure. Separately, the mesothelioma cells were made to overproduce miR-30d.
• Main results:
  • Relative miR-30d level in the pleural mesothelioma cell line NCI-H2452 was 0.671 compared with normal MeT-5A cells.
  • Relative plasma miR-30d level in the 78 asbestos-exposed people was 0.766 compared with the 39 controls (no P value is given in the text).
  • In chrysotile-treated MeT-5A cells, relative miR-30d levels were 0.705 at 24 h, 0.538 at 48 h, 0.775 at 72 h, 0.808 at 8 weeks and 0.484 at 32 weeks, compared with untreated control cells.
  • Chrysotile reduced MeT-5A cell viability at 24 h in a concentration-dependent way. The reduction was significant at 10 micrograms per square centimetre. There was no significant effect at 5 micrograms per square centimetre after 24, 48 or 72 h.
  • Compared with control-treated cells, relative proliferation of NCI-H2452 cells overproducing miR-30d was 90.97% at 24 h, 89.37% at 48 h and 88.06% at 72 h.
  • Overproducing miR-30d inhibited migration and invasion of NCI-H2452 cells compared with control cells.
  • In NCI-H2452 cells, overproducing miR-30d did not significantly arrest the cell cycle. Early apoptosis and the total apoptosis rate increased.
  • In NCI-H2452 cells overproducing miR-30d, CDH1 gene activity rose, while VIM (vimentin) and TWIST1 gene activity fell.
  • At the protein level, CDH1 was not significantly changed, while VIM and TWIST1 proteins were reduced.
• The authors' conclusion: The authors concluded that miR-30d is related to asbestos exposure and inhibits cell migration and invasion by regulating the epithelial–mesenchymal transition in NCI-H2452 cells. They suggested miR-30d could be a tumor suppressor and that its reduction might contribute to pleural mesothelioma and asbestos carcinogenesis.
• Limitations the authors state:
  • The unexposed participants may have been exposed to asbestos in the environment, and this influence could not be eliminated.
  • The plasma difference was modest (0.766), and miR-30d levels in the two groups overlapped.
  • The number of subjects was limited, and more subjects are needed to validate the plasma findings.

Topics

Medical terms in this study, explained in our Lexicon: Asbestos Exposure, Mesothelioma, Latency, Mesothelial Cells, Apoptosis.

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