Interconnected DNA strands protect skin cells from cancer.

Decoding Skin Cancer: How Gene Interactions Influence Your Risk

Nico Varela in Health & Wellness November 2025 • 4 min read.

"Unraveling the connection between RNASEL, MIR146A, and non-melanoma skin cancer (NMSC) to understand your susceptibility and take proactive steps."

Non-melanoma skin cancers (NMSC), including basal cell carcinoma (BCC) and squamous cell carcinoma (SCC), are the most common types of cancer in the United States. While often treatable, understanding the factors that increase your risk is crucial for prevention. Recent research sheds light on the complex interplay of genetics, immunity, and inflammation in the development of these cancers.

A groundbreaking study published in PLOS ONE delves into the interaction between two key genes, RNASEL and MIR146A, and their potential influence on NMSC susceptibility. These genes play vital roles in immune and inflammatory pathways, and variations within them could significantly impact your likelihood of developing skin cancer.

This article breaks down the findings of this study, explaining how these genetic interactions work and what they might mean for your personal risk. We'll explore the roles of RNASEL and MIR146A, discuss the study's methodology and results, and offer actionable insights for protecting your skin.

The Genetic Players: RNASEL and MIR146A

Interconnected DNA strands protect skin cells from cancer.

The study focuses on two genes that are critical for immune and inflammatory responses: RNASEL and MIR146A. Let's take a closer look at each of them:

RNASEL (Ribonuclease L): This gene produces an enzyme that breaks down cellular and viral RNA. It's a key player in the body's defense against viral infections, limiting their spread and triggering apoptosis (programmed cell death) in infected cells. Genetic variations in RNASEL have been linked to an increased risk of several cancers.

MIR146A: This is a microRNA (miRNA), a small non-coding RNA that regulates gene expression. MIR146A acts as a modulator of immune and inflammatory responses, coordinating the functions of myeloid cells and lymphocytes. It essentially fine-tunes the immune system to prevent overreactions and maintain balance.
rs2910164 which reduces miR-146a abundance, in turn altering the cellular transcriptome and increasing levels of its targets.
rs486907 Arg to Gln variant has 3-fold reduced enzyme activity, which could enhance virus susceptibility, diminish control of cellular RNA levels, impair the cellular stress response, or induce apoptosis.

The researchers investigated how common variations (single nucleotide polymorphisms, or SNPs) in these two genes might interact to influence NMSC risk. Specifically, they looked at the SNP rs2910164 in MIR146A and the SNP rs486907 in RNASEL.

Implications and Future Directions

This study provides valuable insights into the complex genetic landscape of NMSC. By identifying the interaction between RNASEL and MIR146A, researchers have opened new avenues for understanding skin cancer susceptibility. While further research is needed to fully elucidate the mechanisms involved, these findings highlight the importance of considering gene-gene interactions in risk assessment and prevention strategies.

About this Article -

This article was crafted using a human-AI hybrid and collaborative approach. AI assisted our team with initial drafting, research insights, identifying key questions, and image generation. Our human editors guided topic selection, defined the angle, structured the content, ensured factual accuracy and relevance, refined the tone, and conducted thorough editing to deliver helpful, high-quality information.See our About page for more information.

This article is based on research published under:

DOI-LINK: 10.1371/journal.pone.0093602, Alternate LINK

Title: Rnasel And Mir146A Snp-Snp Interaction As A Susceptibility Factor For Non-Melanoma Skin Cancer

Subject: Multidisciplinary

Journal: PLoS ONE

Publisher: Public Library of Science (PLoS)

Authors: Shohreh F. Farzan, Margaret R. Karagas, Brock C. Christensen, Zhongze Li, Jacquelyn K. Kuriger, Heather H. Nelson

Published: 2014-04-03

Everything You Need To Know

What is the role of the RNASEL gene in the context of non-melanoma skin cancer?

RNASEL is a gene that produces an enzyme called Ribonuclease L, critical for the body's defense against viral infections. It functions by breaking down cellular and viral RNA, limiting viral spread, and triggering apoptosis (programmed cell death) in infected cells. Genetic variations in RNASEL have been linked to an increased risk of several cancers. In the context of non-melanoma skin cancer, a specific variant, rs486907, results in a 3-fold reduction in enzyme activity, potentially increasing virus susceptibility, diminishing control of cellular RNA levels, impairing the cellular stress response, or inducing apoptosis.

How does MIR146A function in the body, and what is the significance of the rs2910164 SNP?

MIR146A is a microRNA (miRNA) that regulates gene expression. Functioning as a modulator of immune and inflammatory responses, MIR146A coordinates the functions of myeloid cells and lymphocytes. It fine-tunes the immune system to prevent overreactions and maintain balance. The SNP rs2910164 in MIR146A reduces its abundance, altering the cellular transcriptome and increasing levels of its targets. Understanding its function helps in exploring non-melanoma skin cancer susceptibility, specifically in relation to its interaction with RNASEL.

What was the main approach of the PLOS ONE study regarding non-melanoma skin cancer?

The study published in PLOS ONE examined the interaction between RNASEL and MIR146A to determine how variations in these genes might influence NMSC risk. Researchers specifically looked at the SNP rs2910164 in MIR146A and the SNP rs486907 in RNASEL. By identifying the interaction between these two genes, it opens new avenues for understanding skin cancer susceptibility.

How might the interaction between RNASEL and MIR146A affect a person's chances of developing non-melanoma skin cancer?

The interaction between RNASEL and MIR146A could influence an individual's susceptibility to non-melanoma skin cancer by affecting immune and inflammatory responses. Variations in RNASEL, such as rs486907, reduce its enzyme activity, potentially increasing virus susceptibility and impairing cellular stress response. Similarly, the SNP rs2910164 in MIR146A reduces its abundance, altering the cellular transcriptome. The combined effect of these genetic variations can disrupt the immune system's balance, impacting the likelihood of developing skin cancer. However, further research is needed to fully elucidate the mechanisms involved.

What are the limitations of the study, and what other areas need further investigation in non-melanoma skin cancer research?

While this study provides valuable insights into the genetic landscape of non-melanoma skin cancer, it is important to note that other genetic and environmental factors also play a significant role. Future research should focus on exploring these additional factors and their interactions to develop more comprehensive risk assessment and prevention strategies. Furthermore, understanding how these genetic interactions translate into specific cellular and molecular mechanisms could lead to the development of targeted therapies for NMSC.