Li Ni, Zhou Chuane, Yang Fan
Department of Oncology, Chongqing Jiulongpo District People's Hospital, Yangjiaping, Jiulongpo District, Chongqing City, 400050, P.R. China.
Department of Oncology, Jianshi County People's Hospital, Enshi Prefecture, Hubei Province, Jianshi County, Enshi Prefecture, Hubei Province, 445300, P.R. China.
Open Med (Wars). 2022 Oct 3;17(1):1559-1567. doi: 10.1515/med-2022-0500. eCollection 2022.
Long non-coding RNA FAM230B and microRNA (miR-1182) have been characterized as critical players in cancer biology, while their roles in colorectal cancer (CRC) are unclear. We predicted that they could interact with each other and therefore explored the interaction between them in CRC. CRC and paired non-tumor tissue samples were collected from 60 CRC patients, and the expression of FAM230B and miR-1182 (premature and mature) in these samples was analyzed with RT-qPCR. The direct interaction between FAM230B and premature miR-1182 was analyzed with RNA-RNA pull-down assay, and the subcellular location of FAM230B was detected with subcellular fractionation assay. The interaction between FAM230B and miR-1182 was explored with overexpression assay, and their roles in regulating CRC cell proliferation, viability, and colony formation were assessed by BrdU assay, MTT assay, and colony formation assay, respectively. We found that FAM230B and premature miR-1182 were highly upregulated in CRC, while mature miR-1182 was downregulated in CRC. FAM230B was detected in both nucleus and cytoplasm, and it directly interacted with miR-1182. FAM230B overexpression increased the expression levels of premature miR-1182 but decreased the expression levels of mature miR-1182 in CRC cells. FAM230B promoted CRC cell proliferation, increased cell viability, accelerated colony formation, and suppressed the role of miR-1182 in inhibiting CRC cell proliferation. In conclusion, FAM230B is upregulated in CRC and it suppresses the maturation of miR-1182 to promote tumor growth.
长链非编码RNA FAM230B和微小RNA（miR-1182）已被证明是癌症生物学中的关键因子，但其在结直肠癌（CRC）中的作用尚不清楚。我们推测它们可能相互作用，因此探索了它们在CRC中的相互作用。收集了60例CRC患者的CRC组织及配对的非肿瘤组织样本，采用RT-qPCR分析这些样本中FAM230B和miR-1182（前体和成熟体）的表达。采用RNA-RNA下拉试验分析FAM230B与前体miR-1182之间的直接相互作用，采用亚细胞分级分离试验检测FAM230B的亚细胞定位。通过过表达试验探索FAM230B与miR-1182之间的相互作用，并分别通过BrdU试验、MTT试验和集落形成试验评估它们在调节CRC细胞增殖、活力和集落形成中的作用。我们发现FAM230B和前体miR-1182在CRC中高度上调，而成熟miR-1182在CRC中下调。FAM230B在细胞核和细胞质中均有检测到，并且它直接与miR-1182相互作用。FAM230B过表达增加了CRC细胞中前体miR-1182的表达水平，但降低了成熟miR-1182的表达水平。FAM230B促进CRC细胞增殖，增加细胞活力，加速集落形成，并抑制miR-1182在抑制CRC细胞增殖中的作用。总之，FAM230B在CRC中上调，它抑制miR-1182的成熟以促进肿瘤生长。
