TROP2 translation mediated by dual mA/mG RNA modifications promotes bladder cancer development.

RNA modifications, including adenine methylation (mA) of mRNA and guanine methylation (mG) of tRNA, are crucial for the biological function of RNA. However, the mechanism underlying the translation of specific genes synergistically mediated by dual mA/mG RNA modifications in bladder cancer (BCa) remains unclear. We demonstrated that mA methyltransferase METTL3-mediated programmable mA modification of oncogene trophoblast cell surface protein 2 (TROP2) mRNA promoted its translation during malignant transformation of bladder epithelial cells.

sp. Hbc-6 alters physiological metabolism and recruits beneficial rhizosphere bacteria to improve plant growth and drought tolerance.

Drought poses a serious threat to plant growth. Plant growth-promoting bacteria (PGPB) have great potential to improve plant nutrition, yield, and drought tolerance. is an important microbiota genus that is extensively distributed in the plant or rhizosphere.

Expression and prognostic value of SULT1A2 in bladder cancer.

Sulfotransferase Family 1A Member 2 (SULT1A2) is a protein coding gene. Several studies have reported that SULT1A2 may have a chemical carcinogenic effect if expressed as a functional protein. The present study aimed to investigate the expression and potential role of SULT1A2 in bladder cancer (BC).

ALKBH5-mA-FOXM1 signaling axis promotes proliferation and invasion of lung adenocarcinoma cells under intermittent hypoxia.

Obstructive sleep apnea (OSA) is closely associated with cancer progression and cancer-related mortality. N6-methyladenosine (mA) is involved in the process of intermittent hypoxia (IH) promoting tumor progression. However, it is unclear how mA regulates the development of lung adenocarcinoma under IH.

N-methyladenosine modification of ITGA6 mRNA promotes the development and progression of bladder cancer.

Background: Accumulating evidence has revealed the critical roles of N-methyladenosine (mA) modification of mRNA in various cancers. However, the biological function and regulation of mA in bladder cancer (BC) are not yet fully understood.

Methods: We performed cell phenotype analysis and established in vivo mouse xenograft models to assess the effects of mA-modified ITGA6 on BC growth and progression.

Dynamic mA mRNA methylation reveals the role of METTL3-mA-CDCP1 signaling axis in chemical carcinogenesis.

N6-methyladenosine (mA) is the most abundant internal modification in mammalian mRNAs. Despite its functional importance in various physiological events, the role of mA in chemical carcinogenesis remains largely unknown. Here we profiled the dynamic mA mRNA modification during cellular transformation induced by chemical carcinogens and identified a subset of cell transformation-related, concordantly modulated mA sites.