Abstract

Telomerase (TERT) functions to extend the telomeric repeat terminus of each chromosome allowing embryonic cells to proliferate into an adult organism. The TERT gene is subsequently inactivated following maturation, consequently conveying a finite lifespan to every adult cell line, as shortened chromosome arms trigger cell apoptosis. This process ensures that older cells lines, which are invariably accumulating mutations, are eliminated from the body and replaced by stem cells containing founding DNA. One of the defining attributes of a cancer cell is the ability to divide perpetually. This capability to divide continually is often due to the reactivation of TERT. Therefore, the abolishment of TERT activity presents a promising avenue for cancer treatment. Here, we demonstrate through qRT-PCR and ELISA techniques that although small interference RNA (siRNA) results in a transcription knockdown of ninety-seven percent the actual protein activity reduction is far less dramatic. KEYWORDS: Telomerase; Small Interference RNA; Cancer; Tumor; hTERT; qRT-PCR; RNA Interference; ELISA

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