Previous study suggests that miR-148a is involved in the anti-metastasis of HCC cells by the inhibitions of Wnt1-mediated EMT and acquirement of CSCs-like properties. Here, by using TargetScan 6.2, we found that miR-148a was predicted to bind the SMAD2-39 UTR. Moreover, knockdown of miR-148a led to significant increases of the expression/activation of SMAD2 and CSCs-like properties in GLA-treated HepG2 cells. Further, overexpression of miR-148a decreased the expression/activation of SMAD2 and CSC-like properties in Huh-7 and MHCC97H cells. These results suggested that the inhibition of SMAD2 by miR-148a might mediate the GLA-attenuated CSCs-like properties in HCC cells. In conclusion, GLA attenuated the CSCs-like properties by the inhibition of TGF-b/SMADs pathway. Indeed, GLA improved the expression of miR-148a, which targeted the SMAD2-39UTR and down-regulated the SMAD2 expression/activation. Knockdown of miR-148a abolished the GLA-induced inhibition of TGFb/ SMAD2 and the CSCs-like properties in HCC cells. Understanding a novel mechanism, by which GLA inhibits the CSCs-like properties of HCC cells, our study may help to identify potential targets for the therapies of HCC. Ipratropium bromide monohydrate mGluRs comprise a basic characteristic architecture: a large bilobed extracellular amino-terminal domain also known as ����venus fly trap���� with a specific sequence of 24 amino acid for glutamate 4-Hydroxytamoxifen binding site, a 70 amino acid cysteine-rich domain required for dimerization after activation, followed by classic seven alpha-helical transmembrane domain, and an intracellular cytoplasmic tail domain. Various isoforms of Group I mGluRs have been identified depending on the length of C-terminal domain. This C-terminal domain comprises a proline-rich Homer1 binding motif, which involves in intricate protein-protein interactions and complex formation with downstream molecules. Truncation of CTD leads to the loss of Homer1 binding motif in isoforms b-d and thus affects the interaction with other downstream signaling molecules and pathways. Presence of different length isoforms of GRM1 gene with varying role in subsequent activation of downstream signaling pathways, highlight the importance of splicing mechanisms in GRM1 gene function. mGluRs signaling was initially implicated in cellular proliferation of glioma cells and melanoma development either in in vitro or in vivo studies and subsequently this receptor was shown to play a crucial role in various types of cancers Oncogenic function of mGluR1 was shown by the induction of transformed phenotype with overexpression of GRM1 gene in melanocytes.