The interplay of p16INK4a and non-coding RNAs: bridging cellular senescence, aging, and cancer.

Ashok Kumar Balaraman, Muhammad Afzal, Ehssan Moglad, M Arockia Babu, G Padma Priya, Pooja Bansal, Sumit Rajotiya, Benod Kumar Kondapavuluri, Imran Kazmi, Sami I Alzarea, Kavita Goyal, Haider Ali

Research and Enterprise, University of Cyberjaya, Persiaran Bestari, Cyber 11, 63000, Cyberjaya, Selangor, Malaysia.Research and Enterprise, University of Cyberjaya, Persiaran Bestari, Cyber 11, 63000, Cyberjaya, Selangor, Malaysia. · pubmed

Paper

Abstract

p16INK4a is a crucial tumor suppressor and regulator of cellular senescence, forming a molecular bridge between aging and cancer. Dysregulated p16INK4a expression is linked to both premature aging and cancer progression, where non-coding RNAs (ncRNAs) such as long non-coding RNAs (lncRNAs), microRNAs (miRNAs), and small interfering RNAs (siRNAs) play key roles in modulating its function. These ncRNAs interact with p16INK4a through complex post-transcriptional and epigenetic mechanisms, influencing pathways critical to senescence and tumor suppression. In this review, we explore ncRNAs, including ANRIL, MIR31HG, UCA1, MALAT1, miR-24, miR-30, and miR-141, which collectively regulate p16INK4a expression, promoting or inhibiting pathways associated with cancer and aging. ANRIL and MIR31HG modulate p16INK4a silencing via interactions with polycomb repressive complexes (PRC), while miRNAs such as miR-24 and miR-30 target p16INK4a to influence cellular proliferation and senescence. This regulatory interplay underscores the therapeutic potential of ncRNA-targeted strategies to restore p16INK4a function. We summarize recent studies supporting that ncRNAs that control p16INK4a may be diagnostic biomarkers and therapeutic targets for age-related diseases and cancer.

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Research summary

The paper discusses the regulatory role of non-coding RNAs in modulating p16INK4a expression, which is linked to cellular senescence and cancer. This research is relevant as it explores mechanisms that could potentially address the root causes of aging and age-related diseases through the modulation of key regulatory pathways.

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