N6-methyladenosine (m6A) reader LRPPRC-mediated CXCL11 induces cell inflammation to drive breast cancer cell malignancy

Background: Breast cancer (BC) is among the most prevalent malignant cancers in women. This paper proposed to investigate the function as well as the regulatory mechanism of N6-methyladenosine (m6A) reader leucine rich pentatricopeptide repeat containing (LRPPRC) in BC inflammation and progression. Methods: The levels of LRPPRC and C-X-C motif chemokine ligand 11 (CXCL11) were detected via qRT-PCR. The regulatory mechanisms between LRPPRC and CXCL11 were investigated by RIP, MeRIP, and mRNA stability experiments. Moreover, the bio-functions of LRPPRC and CXCL11 in BC cells were explored through the CCK8, wound healing, Transwell assays. ELISA was utilized to evaluate pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) levels. Results: LRPPRC had a considerably higher level in BC samples than in healthy samples, and LRPPRC overexpression predicted poor prognosis. LRPPRC lowexpression diminished BC cell viability, migration, and invasion, whereas overexpression facilitated malignancy. LRPPRC exerted its stimulative effect through CXCL11 m6A modification. CXCL11 upregulating suppressed the LRPPRC silencing’s antitumor effect on BC cells malignancy. CXCL11 upregulation enhances inflammatory factors secretion by BC cells. Conclusion: This study demonstrated that LRPPRC aggravated BC inflammation and malignancy by upregulating m6A modification of CXCL11. These findings offered a potential to be a target for BC patients’ therapy.