Cancer cells showing an increased RNA transcript length compared to normal cells is most likely due to:

INI-CET EXAM -2025

Pathology & Genetics

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Appeared in: INI-CET EXAM -2025

Explanation

Alternative RNA splicing is a process where exons from a pre-mRNA are joined in different combinations to create various mature mRNA molecules.
In cancer, the regulation of splicing is often disrupted.
This disruption can cause exons that are normally excluded in healthy cells to be included in the final mRNA.
The inclusion of these additional exons results in a longer mRNA transcript, which can lead to the production of an altered protein that may contribute to cancer progression.

Option A: Polyadenylation is the addition of a poly(A) tail to the 3' end of an mRNA. While alternative polyadenylation can create transcripts of different lengths, alternative splicing of the main transcript body is a more significant and common cause of the length differences observed in cancer.
Option C: Gene amplification increases the quantity (number of copies) of a gene, leading to more RNA transcripts being produced, but it does not alter the length of each individual transcript.
Option D: Gene silencing is the inhibition of gene expression. It would lead to fewer or no RNA transcripts, which is the opposite of what the question implies.

Visual 1: Diagram - A flowchart comparing normal splicing and alternative splicing. The 'normal' path shows a pre-mRNA with three exons, where Exon 2 is spliced out, resulting in a short mRNA. The 'alternative/cancer' path shows the same pre-mRNA, but all three exons are included, resulting in a longer mRNA. This visually demonstrates how including an extra exon increases transcript length.

Clinical Relevance

Nursing practice connection: This is primarily an exam-oriented knowledge point with limited direct bedside application, so retain Regulation of gene expression and RNA processing in cancer as background academic context rather than a clinical decision trigger.
The altered proteins resulting from alternative splicing in cancer can act as neoantigens or promote cell survival, proliferation, and metastasis.
These unique splice variants are being investigated as cancer-specific biomarkers for diagnosis and prognosis.
Therapeutic strategies are being developed to target the cancer-specific splicing machinery or the abnormal protein products, offering a potential new class of anti-cancer drugs.

How to Approach the Question

First, understand the core of the question: it's asking for a mechanism that can increase the length of an RNA molecule in cancer cells compared to normal cells.
Define each of the four options in the context of molecular biology.
Evaluate the effect of each process on the physical length of an RNA transcript.
Polyadenylation adds a tail, but doesn't change the core transcript.
Gene amplification changes the quantity, not the length.
Gene silencing reduces the amount of transcript.

Concept Tested & Keywords

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