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10.1186/s12964-017-0179-9 http://scihub22266oqcxt.onion/10.1186/s12964-017-0179-9 C5469134!5469134!28606091     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28606091&cmd=llinks): Failed to open stream: HTTP request failed! 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LASP2 suppresses colorectal cancer progression through JNK/p38 MAPK pathway meditated epithelial-mesenchymal transition |pdf=|usr=}}{{28606091}} gab.com Text LASP2 suppresses colorectal cancer progression through JNK/p38 MAPK pathway meditated epithelial-mesenchymal transition JO: Cell Commun Signal http://www.kidney.de/pget.php?&tw=1&pmid=28606091 #FOAvip Background: LASP2 (LIM and SH3 Protein 2) is a small focal adhesion protein belongs to nebulin protein family. As the newest member of nebulette family, the function of LASP2 remains to be identified. Methods: The relationship between LASP2 expression and clinical characteristics of CRC was analyzed in 89 paraffin-embedded archived CRC specimens by immunohistochemistry (IHC). The effects of LASP2 on cell growth and migration were examined in vitro, using CCK-8 and transwell assays. Western blotting was performed to examine the impact of LASP2 on the SAPK/JNK and MAPK signaling pathways. Results: In the present study, we observed a decreased LASP2 expression in clinical colorectal cancer samples compared with paired normal tissues. A negative correlation was also found between LASP2 and poor prognosis of CRC patients. Gain- and loss-of-function approaches revealed that LASP2 plays inhibitory effects on the growth and migration of human CRC cells in vitro. Western-blot results showed that LASP2 could attenuate epithelial-mesenchymal transition (EMT) to accomplish its suppression on CRC aggression. In LASP2 knocked down CRC cells, EMT was inhibited along with the inactivation of JNK/p38 MAPK pathway. Consistently, treatment of JNK inhibitor (JNK inhibitor II) together with p38 inhibitor (SB203580) could resume the process of EMT. Interestingly, we found a negative relationship between LASP2 and LASP1 expression in both CRC cell lines and tumors tissues, which suggests their converse function in CRC progression. Conclusions: All the findings indicated that LASP2 may play a significant role in suppressing CRC progression and provided a novel biomarker for CRC therapy. Electronic supplementary material: The online version of this article (doi:10.1186/s12964-017-0179-9) contains supplementary material, which is available to authorized users. Twit Text FOAVip LASP2 suppresses colorectal cancer progression through JNK/p38 MAPK pathway meditated epithelial-mesenchymal transition ????Cell Commun Signal http://www.kidney.de/pget.php?&tw=1&pmid=28606091 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28606091 #FOAvip English Wikipedia <ref>{{Cite pmid|28606091}}</ref> LASP2 suppresses colorectal cancer progression through JNK/p38 MAPK pathway meditated epithelial-mesenchymal transition #MMPMID28606091 Wang B; Zhang L; Zhao L; Zhou R; Ding Y; Li G; Zhao L Cell Commun Signal 2017[]; 15 (ä): ä PMID28606091show ga Background: LASP2 (LIM and SH3 Protein 2) is a small focal adhesion protein belongs to nebulin protein family. As the newest member of nebulette family, the function of LASP2 remains to be identified. Methods: The relationship between LASP2 expression and clinical characteristics of CRC was analyzed in 89 paraffin-embedded archived CRC specimens by immunohistochemistry (IHC). The effects of LASP2 on cell growth and migration were examined in vitro, using CCK-8 and transwell assays. Western blotting was performed to examine the impact of LASP2 on the SAPK/JNK and MAPK signaling pathways. Results: In the present study, we observed a decreased LASP2 expression in clinical colorectal cancer samples compared with paired normal tissues. A negative correlation was also found between LASP2 and poor prognosis of CRC patients. Gain- and loss-of-function approaches revealed that LASP2 plays inhibitory effects on the growth and migration of human CRC cells in vitro. Western-blot results showed that LASP2 could attenuate epithelial-mesenchymal transition (EMT) to accomplish its suppression on CRC aggression. In LASP2 knocked down CRC cells, EMT was inhibited along with the inactivation of JNK/p38 MAPK pathway. Consistently, treatment of JNK inhibitor (JNK inhibitor II) together with p38 inhibitor (SB203580) could resume the process of EMT. Interestingly, we found a negative relationship between LASP2 and LASP1 expression in both CRC cell lines and tumors tissues, which suggests their converse function in CRC progression. Conclusions: All the findings indicated that LASP2 may play a significant role in suppressing CRC progression and provided a novel biomarker for CRC therapy. Electronic supplementary material: The online version of this article (doi:10.1186/s12964-017-0179-9) contains supplementary material, which is available to authorized users. äLASP2 suppresses colorectal cancer progression through JNK/p38 MAPK pa(epmc).pdf DeepDyve Pubget Overpricing