MiR-373在多种肿瘤中均出现异常表达，扮演着癌基因或者抑癌基因的角色，影响肿瘤细胞的增殖、侵袭和转移过程。有研究报道miR-373在乳腺癌中表达上调，通过下调CD44的表达而促进肿瘤细胞的侵袭转移能力。在人纤维肉瘤HT1080细胞中，过表达的miR-373可直接通过靶向结合雷帕霉素靶蛋白(mechanistic target of rapamycin, mTOR)和去乙酰化酶1(sirtuin 1, SIRT1)mRNA的 3 UTR而使mTOR和SIRT1的表达下调，进一步导致Ras/Raf/MEK/Erk信号通路和转录因子(nuclear factor kappa B, NF-κB)的激活，从而提高MMP-9的表达水平，增强肿瘤细胞的生长和迁移能力。Zhang等研究发现miR-373在胃癌中高表达，通过下调靶基因肿瘤坏死因子α诱导蛋白1(tumor necrosis factor, alpha-induced protein 1, TNFAIP1)的表达而促进胃癌细胞的增殖。然而，miR-373与肺癌的研究甚少，两者的关系尚未十分明确。

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.