As the most common subtype of lung cancer, lung adenocarcinoma (LUAD) is the frequently occurred cancers in human. Therefore, thorough investigation is necessary for understanding the progression of LUAD. HMMR has functioned as a regulator in some cancers, whereas its biological role still needs to be investigated in LUAD. By bioinformatics analysis, we found that HMMR was highly expressed in LUAD tissues and associated with patients' poor prognosis. Further, qRT-PCR demonstrated that HMMR was up-regulated in LUAD tissues and cells. Loss-of-function assays manifested that HMMR knockdown refrained cell proliferation, migration and invasion and enhanced cell apoptosis in LUAD. Later, HMMR was identified as a target gene of miR-34a-5p, which expressed at a low level in LUAD cell and played an anti-oncogenic role in LUAD. Simultaneously, we discovered that miR-34a-5p could directly bind to HCG18. Subsequent assays revealed that HCG18 mediated HMMR expression by sequestering miR-34a-5p. At last, rescue assays proved the carcinogenic role of HCG18/miR-34a-5p/HMMR axis in LUAD cells growth. Importantly, HCG18 was found to facilitate tumor growth in LUAD. Conclusively, HCG18 acted an oncogene in LUAD and enhanced LUAD progression by targeting miR-34a-5p/HMMR axis.
Keywords: HCG18; HMMR; Lung adenocarcinoma; miR-34a-5p.
Copyright © 2020. Published by Elsevier Masson SAS.