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MASTL promotes lenvatinib resistance and the proliferation of HCC cells in vitro and in vivo. (A) Immunoblot (top panel) and qRT-PCR (bottom panel) results showing the relative MASTL expression in various HCC cell lines. (B) Immunoblot and qRT-PCR results showing the efficiency of MASTL overexpression in MHCC97H cells and MASTL-knockdown in <t>SNU449</t> cells. (C) IC 50 values of lenvatinib in MASTL-overexpressing, MASTL-knockdown, and control cell lines. (D) Colony formation assay of MASTL-overexpressing, MASTL-knockdown, and control cell lines treated with lenvatinib in 6-well plates for 12 days. (E–H) Subcutaneous tumor models were established using the indicated cells, and the mice were treated with lenvatinib or vehicle (n=6). Tumor volumes were measured at the indicated time points, and tumor weights were measured at the endpoint. (I) Bubble plot displaying the results of the KEGG pathway analysis of MASTL-overexpressing cell lines. (J) Immunoblot analysis of MAPK signaling pathway activation in the indicated cell lines. (K) Bubble plot showing the results of the GO: BP analysis of MASTL-overexpressing cell lines. (L) Differential bidirectional chart showing the top 10 upregulated and downregulated genes in the “regulation of cell growth” gene set from the GO: BP analysis. All the experiments were repeated a minimum of 3 times. p <0.05 was considered to indicate statistical significance. * p <0.05, ** p <0.01, *** p <0.001. Abbreviations: BP, biological process; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK, mitogen-activated protein kinase; MASTL, microtubule-associated serine/threonine kinase-like; qRT-PCR, quantitative reverse-transcription PCR.
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MASTL promotes lenvatinib resistance and the proliferation of HCC cells in vitro and in vivo. (A) Immunoblot (top panel) and qRT-PCR (bottom panel) results showing the relative MASTL expression in various HCC cell lines. (B) Immunoblot and qRT-PCR results showing the efficiency of MASTL overexpression in MHCC97H cells and MASTL-knockdown in SNU449 cells. (C) IC 50 values of lenvatinib in MASTL-overexpressing, MASTL-knockdown, and control cell lines. (D) Colony formation assay of MASTL-overexpressing, MASTL-knockdown, and control cell lines treated with lenvatinib in 6-well plates for 12 days. (E–H) Subcutaneous tumor models were established using the indicated cells, and the mice were treated with lenvatinib or vehicle (n=6). Tumor volumes were measured at the indicated time points, and tumor weights were measured at the endpoint. (I) Bubble plot displaying the results of the KEGG pathway analysis of MASTL-overexpressing cell lines. (J) Immunoblot analysis of MAPK signaling pathway activation in the indicated cell lines. (K) Bubble plot showing the results of the GO: BP analysis of MASTL-overexpressing cell lines. (L) Differential bidirectional chart showing the top 10 upregulated and downregulated genes in the “regulation of cell growth” gene set from the GO: BP analysis. All the experiments were repeated a minimum of 3 times. p <0.05 was considered to indicate statistical significance. * p <0.05, ** p <0.01, *** p <0.001. Abbreviations: BP, biological process; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK, mitogen-activated protein kinase; MASTL, microtubule-associated serine/threonine kinase-like; qRT-PCR, quantitative reverse-transcription PCR.

Journal: Hepatology (Baltimore, Md.)

Article Title: The MASTL/YBX1/PAK4 axis regulated by stress-activated STK24 triggers lenvatinib resistance and tumor progression in HCC

doi: 10.1097/HEP.0000000000001392

Figure Lengend Snippet: MASTL promotes lenvatinib resistance and the proliferation of HCC cells in vitro and in vivo. (A) Immunoblot (top panel) and qRT-PCR (bottom panel) results showing the relative MASTL expression in various HCC cell lines. (B) Immunoblot and qRT-PCR results showing the efficiency of MASTL overexpression in MHCC97H cells and MASTL-knockdown in SNU449 cells. (C) IC 50 values of lenvatinib in MASTL-overexpressing, MASTL-knockdown, and control cell lines. (D) Colony formation assay of MASTL-overexpressing, MASTL-knockdown, and control cell lines treated with lenvatinib in 6-well plates for 12 days. (E–H) Subcutaneous tumor models were established using the indicated cells, and the mice were treated with lenvatinib or vehicle (n=6). Tumor volumes were measured at the indicated time points, and tumor weights were measured at the endpoint. (I) Bubble plot displaying the results of the KEGG pathway analysis of MASTL-overexpressing cell lines. (J) Immunoblot analysis of MAPK signaling pathway activation in the indicated cell lines. (K) Bubble plot showing the results of the GO: BP analysis of MASTL-overexpressing cell lines. (L) Differential bidirectional chart showing the top 10 upregulated and downregulated genes in the “regulation of cell growth” gene set from the GO: BP analysis. All the experiments were repeated a minimum of 3 times. p <0.05 was considered to indicate statistical significance. * p <0.05, ** p <0.01, *** p <0.001. Abbreviations: BP, biological process; GO, Gene Ontology; KEGG, Kyoto Encyclopedia of Genes and Genomes; MAPK, mitogen-activated protein kinase; MASTL, microtubule-associated serine/threonine kinase-like; qRT-PCR, quantitative reverse-transcription PCR.

Article Snippet: The PLC/PRF/5 and SNU449 cell lines were obtained from the American Type Culture Collection (ATCC), while the MHCC97H cell line was sourced from the Chinese Academy of Sciences.

Techniques: In Vitro, In Vivo, Western Blot, Quantitative RT-PCR, Expressing, Over Expression, Knockdown, Control, Colony Assay, Activation Assay, Reverse Transcription