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p90 ribosomal S6 kinase: a potential therapeutic target in lung cancer

Our plain-English summary of p90 ribosomal S6 kinase: a potential therapeutic target in lung cancer, by N. Poomakkoth, A. Issa, N. Abdulrahman, et al (Journal of Translational Medicine, 2016).

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The study

Abstract

A global survey of cancer has shown that lung cancer is the most common cause of the new cancer cases and cancer deaths in men worldwide. The mortality from lung cancer is more than the combined mortality from breast, prostate and colorectal cancers. The two major histological types of lung cancer are non-small cell lung cancer (NSCLC) accounting for about 85 % of cases and small cell lung cancer accounting for 15 % of cases. NSCLC, the more prevalent form of lung cancer, is often diagnosed at an advanced stage and has a very poor prognosis. Many factors have been shown to contribute to the development of lung cancer in humans including tobacco smoking, exposure to environmental carcinogens (asbestos, or radon) and genetic factors. Despite the advances in treatment, lung cancer remains one of the leading causes of cancer death worldwide. Interestingly, the overall 5 year survival from lung cancer has not changed appreciably in the past 25 years. For this reason, novel and more effective treatments and strategies for NSCLC are critically needed. p90 ribosomal S6 kinase (RSK), a serine threonine kinase that lies downstream of the Ras-MAPK (mitogen activated protein kinase) cascade, has been demonstrated to be involved in the regulation of cell proliferation in various malignancies through indirect (e.g., modulation of transcription factors) or direct effects on the cell-cycle machinery. Increased expression of RSK has been demonstrated in various cancers, including lung cancer. This review focuses on the role of RSK in lung cancer and its potential therapeutic application.

In plain English

This article was a review, not an original study. The authors summarized published research on p90 ribosomal S6 kinase (RSK), a protein the review describes as lying downstream of the Ras-MAPK signaling pathway and helping regulate cell growth, division and survival. Its focus was lung cancer, especially lung adenocarcinoma. Asbestos appeared only once, in the abstract, listed with radon as an environmental carcinogen that contributes to lung cancer. The review did not examine asbestos exposure. Citing other researchers' work, the review reported that RSK is overexpressed or overactive in several cancers, including lung cancer. It reported that Lara and colleagues observed RSK4 overexpressed in more than 50% of primary malignant lung cancers. It also described experimental drugs that block RSK. The authors mentioned their own unpublished data, with no figures given, linking an RSK inhibitor to reduced migration and proliferation of A549 lung adenocarcinoma cells. The authors concluded that RSKs might prove to be promising targets for treating lung adenocarcinomas. They noted that the exact role of each RSK form in lung cancer remains unknown and that further studies 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: Narrative review of published literature on RSK in lung cancer; no methods for selecting studies are described
  • Who was studied: No study population. The review covered published laboratory and clinical literature on lung cancer, with emphasis on lung adenocarcinoma.
  • Exposure: Asbestos was not studied. It was mentioned once, with radon, as an environmental carcinogen among factors contributing to lung cancer. The review's subject was the RSK protein kinase and drugs that inhibit it.
  • Main results:
    • Citing earlier work, the review reported that RSKs are overexpressed or hyperactivated in several cancers, including lung cancer.
    • Citing Lara and colleagues, the review reported that RSK4 is overexpressed in more than 50% of primary malignant lung cancers, though undetectable in normal cells.
    • Citing earlier work, the review reported that knocking down RSK isoform 1 increased the metastatic potential of A549 lung adenocarcinoma cells. It also reported that RSK2 and RSK4 were linked to increased migration of these cells.
    • The authors reported their own unpublished data, without figures: exposing A549 lung adenocarcinoma cells to the RSK inhibitor BI-D1870 decreased RSK1 protein expression and was associated with decreased cell migration and proliferation.
  • The authors' conclusion: The authors concluded that RSKs might prove to be promising targets in the chemotherapy of lung adenocarcinomas, particularly those with oncogenic mutations in the Ras signaling pathway.
  • Limitations the authors state:
    • The authors stated that the exact role and signaling pathway of the different RSK forms in lung cancer remain unknown.
    • The authors stated that further studies are needed to verify whether RSK inhibitors work, alone or combined with other anti-cancer agents, in lung cancer.

Topics

The National Library of Medicine indexes this study under subjects our site covers: Lung cancer.

Medical terms in this study, explained in our Lexicon: Lung Cancer, Colorectal Cancer, Non-Small Cell Lung Cancer, Small Cell Lung Cancer, Prognosis.

Browse more research in Journal of Translational Medicine, or return to medical research.

Cited on this site

How to cite it

Cite the study

N. Poomakkoth, A. Issa, N. Abdulrahman, S.G. Abdelaziz, F. Mraiche. p90 ribosomal S6 kinase: a potential therapeutic target in lung cancer. Journal of Translational Medicine 2016;14:14. doi:10.1186/s12967-016-0768-1. PMID: 26791782.

Cite our summary

“p90 ribosomal S6 kinase: a potential therapeutic target in lung cancer.” AsbestosClaims.Law Library. https://asbestosclaims.law/library/research/p90-ribosomal-s6-kinase-a-potential-therapeutic-target-in-lung-cancer.

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