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. 2021 Jun 9;11:670917. doi: 10.3389/fonc.2021.670917

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Copyright © 2021 Ghafouri-Fard, Agabalazadeh, Abak, Shoorei, Hassanzadeh Taheri, Taheri and Sharifi

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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A schematic illustration of the crosstalk between lncRNAs and Wnt/β-catenin pathway involved in the modulation of the sensitivity of glioma cells to chemotherapeutic agents. Downregulation of lncRNA H19 could promote the sensitivity of glioma cells to temozolomide via inhibiting EMT through the suppression of the Wnt/β-Catenin signaling cascade. Silencing of H19 could downregulate the expression level of β-catenin and its downstream targets c-myc and Survivin in temozolomide-treated glioma cells (11). Besides, downregulating the expression of lncRNA MIR22HG could suppress the Wnt/β-catenin signaling pathway via loss of miR-22-3p and -5p. This could in turn lead to attenuating cell proliferation, invasion as well as tumor growth in glioma cells. MIR22HG silencing could result in downregulating the expression level of β-catenin, a key transcriptional regulator of Wnt, along with the inhibition of several Wnt downstream targets, containing c-Myc, cyclin D1, and LEF1, as well as a reduction in the expression of phospho-GSK3β (Ser9) in tumor cells (12). Besides, upregulation of lncRNA MIR155HG could promote temozolomide resistance in glioma cells through directly regulating canonical Wnt/β-catenin pathway activation via binding to PTBP1 in tumor cells (13).