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Long noncoding RNAs (lncRNAs) contribute to many steps in carcinogenesis and often serve as biomarkers or therapeutic targets for tumor diagnosis and therapy. Although the role of lncRNAs in tumor formation is becoming clear, whether lncRNAs mediate gut microbiota-induced colorectal cancer (CRC) is largely unknown. Enterotoxigenic  Bacteroides fragilis  (ETBF) is a well-known tumor-inducing bacterium in the human gut; however, its tumorigenic effect remains to be explored. In the present study, we revealed the mechanism by which a lncRNA participates in gut bacteria-induced carcinogenesis:  Bacteroides fragilis -associated lncRNA1 ( BFAL1 ) in CRC tissues mediates ETBF carcinogenesis.  BFAL1  was highly expressed in CRC tissues compared with that in adjacent normal tissues. In vitro,  BFAL1  was upregulated in ETBF-treated CRC cells. Mechanistically, ETBF promoted tumor growth via  BFAL1  by activating the Ras homolog, which is the MTORC1 binding/mammalian target of the rapamycin (RHEB/mTOR) pathway. Furthermore,  BFAL1  regulated  RHEB  expression by competitively sponging microRNAs miR-155-5p and miR-200a-3p. Clinically, both high expression of  BFAL1  and high abundance of ETBF in CRC tissues predicted poor outcomes for patients with CRC. Thus,  BFAL1  is a mediator of ETBF-induced carcinogenesis and may be a potential therapeutic target for ETBF-induced CRC.

Long noncoding RNA BFAL1 mediates enterotoxigenic Bacteroides fragilis-related carcinogenesis in colorectal cancer via the RHEB/mTOR pathway