miR-206/133b Cluster: A Weapon against Lung Cancer?

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miR-206/133b Cluster: A Weapon against Lung Cancer? Jing-Yu Pan, Cheng-Cao Sun, Zhuo-Yue Bi, Zhen-Long Chen, Shu-Jun Li, Qing-Qun Li, Yu-Xuan Wang, Yong-Yi Bi, De-Jia Li Molecular Therapy - Nucleic Acids Volume 8, Pages 442-449 (September 2017) DOI: 10.1016/j.omtn.2017.06.002 Copyright © 2017 The Author(s) Terms and Conditions

Figure 1 miR-133b/206 Associates with Various Genes Mediating NSCLC Cell Migration and Invasion miR-206 promoted lung cancer cell apoptosis by targeting c-Met and Bcl2, as well as governed EGFR, MET, and its downstream phosphorylation of ERK1/2 and AKT. Likewise, miR-133b boosted lung cancer cell apoptosis by suppressing expression of MCL1, BCL2L2, and attenuated EGFR and its downstream phosphorylation of ERK1/2 and AKT. Furthermore, miR-206 inhibited lung cancer cell migration and invasion by repressing SOX9 and Smad3 and upregulating E-cadherin, meanwhile blocked EGFR, MET, and its downstream phosphorylation of ERK1/2 and AKT, as well as antagonized c-Met and the PI3K/Akt/mTOR pathway. miR-133b repressed FSCN1, contributing to the blockage of lung cancer cell migration and invasion. Molecular Therapy - Nucleic Acids 2017 8, 442-449DOI: (10.1016/j.omtn.2017.06.002) Copyright © 2017 The Author(s) Terms and Conditions

Figure 2 miR-206 Associates with Various Genes Mediating NSCLC Cell Proliferation NRF2 could decrease miR-206 expression, while miR-206 was able to repress the pentose phosphate pathway genes (G6PD, PGD, TKT, and GPD2), reducing pentose phosphate pathway-related NADPH production and ribose synthesis and then giving rise to blockage of lung cancer cell proliferation. In addition, TGF-β1 enabled miR-206 to decline, whereas restoration of miR-206 significantly suppressed the level of Samd3 and TRIB2, leading to inhibit proliferation. However, miR-206 also directly repressed Bcl2 and c-Met expression, contributing to inhibition of cell proliferation in lung cancer. Molecular Therapy - Nucleic Acids 2017 8, 442-449DOI: (10.1016/j.omtn.2017.06.002) Copyright © 2017 The Author(s) Terms and Conditions