MiR-373在多種腫瘤中均出現(xiàn)異常表達(dá)，扮演著癌基因或者抑癌基因的角色，影響腫瘤細(xì)胞的增殖、侵襲和轉(zhuǎn)移過程。有研究報道m(xù)iR-373在乳腺癌中表達(dá)上調(diào)，通過下調(diào)CD44的表達(dá)而促進(jìn)腫瘤細(xì)胞的侵襲轉(zhuǎn)移能力。在人纖維肉瘤HT1080細(xì)胞中，過表達(dá)的miR-373可直接通過靶向結(jié)合雷帕霉素靶蛋白(mechanistic target of rapamycin, mTOR)和去乙酰化酶1(sirtuin 1, SIRT1)mRNA的 3 UTR而使mTOR和SIRT1的表達(dá)下調(diào)，進(jìn)一步導(dǎo)致Ras/Raf/MEK/Erk信號通路和轉(zhuǎn)錄因子(nuclear factor kappa B, NF-κB)的激活，從而提高M(jìn)MP-9的表達(dá)水平，增強(qiáng)腫瘤細(xì)胞的生長和遷移能力。Zhang等研究發(fā)現(xiàn)miR-373在胃癌中高表達(dá)，通過下調(diào)靶基因腫瘤壞死因子α誘導(dǎo)蛋白1(tumor necrosis factor, alpha-induced protein 1, TNFAIP1)的表達(dá)而促進(jìn)胃癌細(xì)胞的增殖。然而，miR-373與肺癌的研究甚少，兩者的關(guān)系尚未十分明確。

miR-373 is abnormally expressed in many types of tumors. It may function as an oncogene or a tumor suppressor gene and influence the proliferation, invasion, and metastasis of tumor cells. Previous studies have reported that miR-373 is upregulated in breast cancer and that it promotes tumor cell invasion and metastasis by downregulating CD44 expression. In HT1080 human fibrosarcoma cells, overexpressed miR-373 may directly target the 3′ UTRs of the mRNAs of mechanistic target of rapamycin (mTOR) and sirtuin 1 (SIRT1). Consequently, mTOR and SIRT1 are downregulated, thereby activating the Ras/Raf/MEK/Erk signaling pathway and the transcription factor nuclear factor kappa B (NF-κB). This results in an increase in matrix metallopeptidase 9 (MMP-9) expression and an enhancement in the growth and migratory abilities of tumor cells. Zhang et al. have shown that miR?373 is upregulated in gastric cancer and that it promotes the proliferation of gastric cancer cells by downregulating tumor necrosis factor, alpha-induced protein 1 (TNFAIP1). However, the relationship between miR 373 and lung cancer remains unclear owing to a lack of relevant research.