Investigator
Central University Of Punjab
m6A modification and its clinical applications in gynaecological cancer
N6-methyladenosine (m6A) RNA modification plays a pivotal role in gynaecological cancers by regulating tumor initiation, progression, and therapeutic resistance. m6A RNA modification include writers (METTL3/14, RBM15, ZC3H13, WTAP), which catalyze methylation; erasers (ALKBH5, FTO), which remove methyl groups; and readers (YTHDC1, YTHDF1/2/3, IGF2BP1/2/3, HNRNPC/G, HNRNPA2BP1), which interpret m6A marks to regulate the RNA fate. These regulators alter basic RNA metabolism, such as splicing, mRNA stability, translation, and degradation. In gynaecological cancers, both oncogenic and tumor suppressive signaling pathways are also altered by these regulators. Due to their diagnostic, prognostic and predictive value, m6A regulators have emerged as promising biomarkers in gynaecological cancers in recent years. This review highlights the role of m6A regulators and critically evaluates their biomarker and clinical potential in gynaecological cancers.
Molecular and bioinformatics analysis of long non-coding RNAs in cervical cancer
Various long non-coding RNAs (lncRNAs) have indicated their role in different regulatory processes and therapeutics in cervical cancer (CC). This study aims to assess the gene expression and methylation status of LINC00518 & MAFG-AS1 in CC patients. Methylation-specific PCR (MS-PCR) and quantitative real-time PCR (qRT-PCR) were performed on 81 patients. The association of the promoter methylation status of cancer tissues was studied with HPV infection and clinicopathological factors. The Kaplan-Meier curves were used from the GEPIA and TANRIC databases to analyze the overall survival of CC patients. The bioinformatics analysis of relative gene expression was carried out using the GEPIA database. The RNAinter database was also explored to find out the potential interacting partners. This is the first-ever research revealing that hypomethylation of the LINC00518 gene promoter may be relevant to its oncogenic behavior in CC (p < 0.05). However, no significant difference was observed between the MAFG-AS1 methylation status of cancerous and normal tissues. A notable association between the methylation status of LINC00518 promoter and clinicopathological factors, including age (p < 0.001), histological subtypes (p < 0.00001), and differentiation degree (p < 0.00001), has been observed, indicating its possible role in predicting the severity and prognosis of this disease. Overall survival analysis showed a significant value for LINC00518 using GEPIA (p < 0.05). Our findings about the gene expression of LINC00518 and its hypomethylated status in cancerous tissues suggest a potential mechanism that might contribute to its dysregulation in CC and could serve as a potential clinical biomarker.
