RAS oncogenes are master regulator genes in many cancers. In general, RAS-driven cancers have an oncogenic RAS mutation that promotes disease progression (colon, lung, pancreas). In contrast, brain tumors are not necessarily RAS-driven cancers because RAS mutations are rarely observed. In particular, glioblastomas (the most lethal brain tumor) do not appear to have dominant genetic mutations that are suitable for targeted therapy. Standard treatment for most brain tumors continues to focus on maximal surgical resection, radiotherapy and chemotherapy. Yet the convergence of genomic aberrations such as EGFR, PDGFR and NF1 (some of which are clinically effective) with activation of the RAS/MAPK cascade is still considered a key point in gliomagenesis, and KRAS is undoubtedly a driving gene in gliomagenesis in mice. In cancer, microRNAs (miRNA) are small, non-coding RNAs that regulate carcinogenesis. However, the functional consequences of aberrant miRNA expression in cancer are still poorly understood. let-7 encodes an intergenic miRNA that is classified as a tumour suppressor, at least in lung cancer. Let-7 suppresses a plethora of oncogenes such as RAS, HMGA, c-Myc, cyclin-D and thus suppresses cancer development, differentiation and progression. let-7 family members are direct regulators of certain RAS family genes by binding to the sequences in their 3′untranslated region (3′UTR). let-7 miRNA is involved in the malignant behaviour in vitro—proliferation, migration and invasion—of gliomas and stem-like glioma cells as well as in vivo models of glioblastoma multiforme (GBM) via KRAS inhibition. It also increases resistance to certain chemotherapeutic agents and radiotherapy in GBM. Although let-7 therapy is not yet established, this review updates the current state of knowledge on the contribution of miRNA let-7 in interaction with KRAS to the oncogenesis of brain tumours.

RAS癌基因是许多癌症的主调控基因。一般来说，RAS驱动的癌症具有致癌的RAS突变，可促进疾病进展（结肠癌、肺癌、胰腺癌）。相反，脑肿瘤不一定是RAS驱动的癌症，因为很少观察到RAS突变。特别是，胶质母细胞瘤（最致命的脑肿瘤）似乎不具有适合靶向治疗的显性基因突变。大多数脑肿瘤的标准治疗仍然集中于最大程度的手术切除、放疗和化疗。然而，EGFR、PDGFR和NF1等基因组畸变（其中一些在临床上有效）与RAS /MAPK级联激活的融合仍然被认为是胶质瘤发生的关键点，而KRAS无疑是小鼠胶质瘤发生的驱动基因。在癌症中，microRNA (miRNA) 是调节癌发生的小型非编码 RNA。然而，癌症中异常 miRNA 表达的功能后果仍知之甚少。let-7编码一种基因间 miRNA，被归类为肿瘤抑制因子，至少在肺癌中是如此。Let-7抑制多种癌基因，如RAS、HMGA、c-Myc、cyclin-D，从而抑制癌症的发生、分化和进展。let-7家族成员通过与其 3' 非翻译区 (3'UTR) 中的序列结合，成为某些RAS家族基因的直接调节因子。 let-7 miRNA 通过抑制KRAS参与神经胶质瘤和干细胞样神经胶质瘤细胞的体外恶性行为（增殖、迁移和侵袭）以及多形性胶质母细胞瘤 (GBM) 的体内模型。它还增加 GBM 对某些化疗药物和放疗的抵抗力。尽管let-7疗法尚未建立，但这篇综述更新了目前关于 miRNA let-7与KRAS相互作用对脑肿瘤发生的贡献的知识状态。