Exploring the molecular pathways of advanced rectal cancer: A focus on genetic, RNA, and biological technique

Colorectal cancer (CRC) is the third most commonly diagnosed cancer in both men and women and ranks as the second leading cause of cancer-related deaths in the United States each year. Among CRC cases, RC accounts for 35 % and presents a significant health concern [1], [2]. While RC predominantly affects older individuals, a notable increase in incidence has been between 40 and 5 years of age [3]. The first step in RC carcinogenesis involves a genetic and epigenetic change that leads to proliferation. These hyper-proliferative cells cause benign adenoma, which further leads to carcinoma and spreads to different organs [4]. The three main pathways—CpG island methylator phenotype (CIMP)—chromosomal instability (CI), and microsatellite instability (MSI) play an important part in the genetic instability and pathophysiology of CRC [5].

Recent molecular biology and genetics breakthroughs have significantly impacted the advancement of various areas within the life and health sciences [6]. The latest technologies have been introduced to study CRC towards the mechanistic study and conventional techniques. These technologies, which include proteomics, metabolomics, transcriptomics, and genomics, clarify proteins, RNA transcripts, DNA markers, and metabolites generated within the colon and rectum regions of the gut [7]. According to recent research, CRC can be detected and its prognosis evaluated using a variety of proteins, extracellular vesicles (exosomes), gene transcripts, particular genetic variants, such as long non-coding RNAs (lncRNAs), microRNAs (miRNAs), cell-free DNA (cfDNA), different epigenetic patterns, and circulating tumor DNA (ctDNA). RNA alterations play a crucial role in various cancers, aided by advanced technologies like mapping and RNA modification. These tools help us gain insights into the biological functions of molecular markers across different cellular contexts [8]. The miRNAs are a new class of therapeutic targets, which show that they act as tumor suppressor and oncogenes and are also observed in various types of human tumors such as CRC [9].

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