2019
DOI: 10.1002/mc.23123
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Abstract: The activation of oncogenic mitogen-activated protein kinase cascade via mutations in BRAF is often observed in human melanomas. Targeted inhibitors of BRAF (BRAFi), alone or as a part of a combination therapy, offer a significant benefit to such patients. Unfortunately, some cases are initially nonresponsive to these drugs, while others become refractory in the course of treatment, underscoring the need to understand and mitigate the underlying resistance mechanisms. We report that interference with polo-like… Show more

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Cited by 7 publications
(5 citation statements)
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References 56 publications
(97 reference statements)
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“…A considerable number of preclinical studies are investigating other novel targets for overcoming BRAF inhibitor resistance. These include combining BRAF and/or MEK inhibitors with inhibitors of pre-mRNA splicing (to counteract resistance caused by BRAF splicing) [ 251 ], BH3-mimetics [ 252 , 253 ], BCL2 inhibitors [ 254 ], mitochondrial-targeted agents [ 255 , 256 ], inhibitors of p90 ribosomal S6 kinases [ 257 , 258 ], pro-caspase activating compounds [ 259 ], Rho kinase 1 (ROCK1) inhibitors [ 260 ], protein kinase Cδ inhibitors [ 261 ], tubulin inhibitors [ 262 ], ErbB2 or ErbB3 inhibitors [ 222 , 263 , 264 ], activators of the liver-X nuclear hormone receptor [ 265 ], an antibody conjugate targeting the endothelin B receptor [ 266 ], monoclonal antibodies against chondroitin sulfate proteoglycan 4 [ 267 ], inhibitors of sterol regulator element binding protein I (SREBP-1) [ 268 ], copper chelators [ 269 ], polo-like 3 kinase inhibitors (including in models of BRAF + MEK inhibitor resistance) [ 270 , 271 ], anti-nodal antibodies [ 272 ], PAK1 inhibitors [ 273 ], GLI1/2 inhibitors [ 274 ], inhibitors of IQ motif-containing GTPase activating protein 1 (IQGAP1) [ 275 ], serotonin agonists [ 276 ], CK2 inhibitors [ 277 ], p53 activators [ 278 ], metformin [ 279 ], statins [ 280 ], non-steroidal anti-inflammatory drugs [ 281 ], mibefradil [ 282 ], hydroxychloroquine (an autophagy inhibitor) [ 83 ], and A100 (a reactive oxygen species-activated prodrug) [ 283 ].…”
Section: Resultsmentioning
confidence: 99%
“…A considerable number of preclinical studies are investigating other novel targets for overcoming BRAF inhibitor resistance. These include combining BRAF and/or MEK inhibitors with inhibitors of pre-mRNA splicing (to counteract resistance caused by BRAF splicing) [ 251 ], BH3-mimetics [ 252 , 253 ], BCL2 inhibitors [ 254 ], mitochondrial-targeted agents [ 255 , 256 ], inhibitors of p90 ribosomal S6 kinases [ 257 , 258 ], pro-caspase activating compounds [ 259 ], Rho kinase 1 (ROCK1) inhibitors [ 260 ], protein kinase Cδ inhibitors [ 261 ], tubulin inhibitors [ 262 ], ErbB2 or ErbB3 inhibitors [ 222 , 263 , 264 ], activators of the liver-X nuclear hormone receptor [ 265 ], an antibody conjugate targeting the endothelin B receptor [ 266 ], monoclonal antibodies against chondroitin sulfate proteoglycan 4 [ 267 ], inhibitors of sterol regulator element binding protein I (SREBP-1) [ 268 ], copper chelators [ 269 ], polo-like 3 kinase inhibitors (including in models of BRAF + MEK inhibitor resistance) [ 270 , 271 ], anti-nodal antibodies [ 272 ], PAK1 inhibitors [ 273 ], GLI1/2 inhibitors [ 274 ], inhibitors of IQ motif-containing GTPase activating protein 1 (IQGAP1) [ 275 ], serotonin agonists [ 276 ], CK2 inhibitors [ 277 ], p53 activators [ 278 ], metformin [ 279 ], statins [ 280 ], non-steroidal anti-inflammatory drugs [ 281 ], mibefradil [ 282 ], hydroxychloroquine (an autophagy inhibitor) [ 83 ], and A100 (a reactive oxygen species-activated prodrug) [ 283 ].…”
Section: Resultsmentioning
confidence: 99%
“…Furthermore, we showed that RPTOR, PLK1, and GRB7 formed a complex, and their knockdown synergistically inhibited CRC cell proliferation with MEKi, consistent with the fact that activation of the mTOR pathway plays a pivotal role in RTKi resistance [ 43 ]. Recently, PLK3, another member of the PLK1 family, was reported to confer resistance to the MAPK pathway inhibitor in melanoma [ 44 ]. Thus, the detailed function of the PLK1 family in the regulation of MEKi resistance in CRCs needs to be further investigated.…”
Section: Discussionmentioning
confidence: 99%
“…Given the enrichment of PLK3 at the plasma membrane and Golgi apparatus, it will be interesting to test its potential impact on cell adhesion and intracellular trafficking that are regulated by PP6 phosphatase [48,49]. Finally, there is emerging evidence that expression of PLK3 could affect the therapeutical response in melanoma, prostate cancer and colon carcinoma [50][51][52]. Further phosphoproteomic studies are needed to identify new substrates of PLK3 that could explain its role in cell physiology and sensitivity to chemotherapy.…”
Section: Discussionmentioning
confidence: 99%