Influence of SHH/GLI1 axis on EMT mediated migration and invasion of breast cancer cells
Sonic Hedgehog signaling is critical for breast morphogenesis and cancer. The present study was conducted to explore the influence of SHH/GLI1 axis on epithelial mesenchymal transition and invasion in breast cancer cells. SHH/GLI1 positive samples demonstrated high expression of Snail and Vimentin w...
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| Veröffentlicht in: | Scientific reports 2019-04, Vol.9 (1), p.6620, Article 6620 |
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| description | Sonic Hedgehog signaling is critical for breast morphogenesis and cancer. The present study was conducted to explore the influence of SHH/GLI1 axis on epithelial mesenchymal transition and invasion in breast cancer cells. SHH/GLI1 positive samples demonstrated high expression of Snail and Vimentin with relatively low expression of E-cadherin. Overexpression of Vimentin and Snail in SHH/GLI1 positive patients was also associated with poor overall survival. Interestingly, GANT61 (GLI1 inhibitor) exposure significantly reduced cell viability and induced apoptosis at 10 µM. Suppression of Hedgehog pathway either by CRISPR mediated SHH knock out or GANT61 altered regulation of EMT markers in breast cancer cells. Moreover, in-activation of SHH/GLI1 axis also significantly restricted cell migration and invasiveness. These findings suggest that targeting SHH/GLI1 axis alters expression of EMT markers and abrogates neoplastic invasion in breast cancer cells. |
| doi_str_mv | 10.1038/s41598-019-43093-x |
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The present study was conducted to explore the influence of SHH/GLI1 axis on epithelial mesenchymal transition and invasion in breast cancer cells. SHH/GLI1 positive samples demonstrated high expression of Snail and Vimentin with relatively low expression of E-cadherin. Overexpression of Vimentin and Snail in SHH/GLI1 positive patients was also associated with poor overall survival. Interestingly, GANT61 (GLI1 inhibitor) exposure significantly reduced cell viability and induced apoptosis at 10 µM. Suppression of Hedgehog pathway either by CRISPR mediated SHH knock out or GANT61 altered regulation of EMT markers in breast cancer cells. Moreover, in-activation of SHH/GLI1 axis also significantly restricted cell migration and invasiveness. These findings suggest that targeting SHH/GLI1 axis alters expression of EMT markers and abrogates neoplastic invasion in breast cancer cells.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-43093-x</identifier><identifier>PMID: 31036836</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/1 ; 13/106 ; 13/109 ; 13/2 ; 13/31 ; 13/44 ; 13/51 ; 13/95 ; 14 ; 14/19 ; 38 ; 631/67/1347 ; 631/80/86/2370 ; 96 ; Adult ; Aged ; Aged, 80 and over ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Breast cancer ; Breast Neoplasms - drug therapy ; Breast Neoplasms - metabolism ; Breast Neoplasms - pathology ; Cadherins - genetics ; Cadherins - metabolism ; Cell adhesion & migration ; Cell migration ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cell Proliferation - genetics ; Cell viability ; CRISPR ; E-cadherin ; Epithelial-Mesenchymal Transition - drug effects ; Epithelial-Mesenchymal Transition - genetics ; Female ; Hedgehog protein ; Humanities and Social Sciences ; Humans ; Invasiveness ; Mesenchyme ; Middle Aged ; Morphogenesis ; multidisciplinary ; Pyridines - pharmacology ; Pyrimidines - pharmacology ; Science ; Science (multidisciplinary) ; Signal Transduction - drug effects ; Snail Family Transcription Factors - genetics ; Snail Family Transcription Factors - metabolism ; Vimentin ; Vimentin - genetics ; Vimentin - metabolism ; Young Adult ; Zinc Finger Protein GLI1 - antagonists & inhibitors ; Zinc Finger Protein GLI1 - genetics ; Zinc Finger Protein GLI1 - metabolism</subject><ispartof>Scientific reports, 2019-04, Vol.9 (1), p.6620, Article 6620</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. 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The present study was conducted to explore the influence of SHH/GLI1 axis on epithelial mesenchymal transition and invasion in breast cancer cells. SHH/GLI1 positive samples demonstrated high expression of Snail and Vimentin with relatively low expression of E-cadherin. Overexpression of Vimentin and Snail in SHH/GLI1 positive patients was also associated with poor overall survival. Interestingly, GANT61 (GLI1 inhibitor) exposure significantly reduced cell viability and induced apoptosis at 10 µM. Suppression of Hedgehog pathway either by CRISPR mediated SHH knock out or GANT61 altered regulation of EMT markers in breast cancer cells. Moreover, in-activation of SHH/GLI1 axis also significantly restricted cell migration and invasiveness. These findings suggest that targeting SHH/GLI1 axis alters expression of EMT markers and abrogates neoplastic invasion in breast cancer cells.</description><subject>13</subject><subject>13/1</subject><subject>13/106</subject><subject>13/109</subject><subject>13/2</subject><subject>13/31</subject><subject>13/44</subject><subject>13/51</subject><subject>13/95</subject><subject>14</subject><subject>14/19</subject><subject>38</subject><subject>631/67/1347</subject><subject>631/80/86/2370</subject><subject>96</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - drug therapy</subject><subject>Breast Neoplasms - metabolism</subject><subject>Breast Neoplasms - pathology</subject><subject>Cadherins - genetics</subject><subject>Cadherins - metabolism</subject><subject>Cell adhesion & migration</subject><subject>Cell migration</subject><subject>Cell Movement - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Riaz, Syeda Kiran</au><au>Ke, Yuepeng</au><au>Wang, Fen</au><au>Kayani, Mahmood Akhtar</au><au>Malik, Muhammad Faraz Arshad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Influence of SHH/GLI1 axis on EMT mediated migration and invasion of breast cancer cells</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-04-29</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>6620</spage><pages>6620-</pages><artnum>6620</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Sonic Hedgehog signaling is critical for breast morphogenesis and cancer. The present study was conducted to explore the influence of SHH/GLI1 axis on epithelial mesenchymal transition and invasion in breast cancer cells. SHH/GLI1 positive samples demonstrated high expression of Snail and Vimentin with relatively low expression of E-cadherin. Overexpression of Vimentin and Snail in SHH/GLI1 positive patients was also associated with poor overall survival. Interestingly, GANT61 (GLI1 inhibitor) exposure significantly reduced cell viability and induced apoptosis at 10 µM. Suppression of Hedgehog pathway either by CRISPR mediated SHH knock out or GANT61 altered regulation of EMT markers in breast cancer cells. Moreover, in-activation of SHH/GLI1 axis also significantly restricted cell migration and invasiveness. These findings suggest that targeting SHH/GLI1 axis alters expression of EMT markers and abrogates neoplastic invasion in breast cancer cells.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31036836</pmid><doi>10.1038/s41598-019-43093-x</doi><orcidid>https://orcid.org/0000-0001-7965-4178</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/1 13/106 13/109 13/2 13/31 13/44 13/51 13/95 14 14/19 38 631/67/1347 631/80/86/2370 96 Adult Aged Aged, 80 and over Apoptosis Apoptosis - drug effects Apoptosis - genetics Breast cancer Breast Neoplasms - drug therapy Breast Neoplasms - metabolism Breast Neoplasms - pathology Cadherins - genetics Cadherins - metabolism Cell adhesion & migration Cell migration Cell Movement - drug effects Cell Proliferation - drug effects Cell Proliferation - genetics Cell viability CRISPR E-cadherin Epithelial-Mesenchymal Transition - drug effects Epithelial-Mesenchymal Transition - genetics Female Hedgehog protein Humanities and Social Sciences Humans Invasiveness Mesenchyme Middle Aged Morphogenesis multidisciplinary Pyridines - pharmacology Pyrimidines - pharmacology Science Science (multidisciplinary) Signal Transduction - drug effects Snail Family Transcription Factors - genetics Snail Family Transcription Factors - metabolism Vimentin Vimentin - genetics Vimentin - metabolism Young Adult Zinc Finger Protein GLI1 - antagonists & inhibitors Zinc Finger Protein GLI1 - genetics Zinc Finger Protein GLI1 - metabolism |
| title | Influence of SHH/GLI1 axis on EMT mediated migration and invasion of breast cancer cells |
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