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Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer
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| Zeitschriftentitel: | Journal of Cellular Biochemistry |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | Journal of Cellular Biochemistry, 121, 2020, 11, S. 4642-4653 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
|
| Schlagwörter: |
| author_facet |
Tang, Xiaojiang Zhou, Yuhui Liu, Yang Zhang, Wei Liu, Chao Yan, Changyou Tang, Xiaojiang Zhou, Yuhui Liu, Yang Zhang, Wei Liu, Chao Yan, Changyou |
|---|---|
| author |
Tang, Xiaojiang Zhou, Yuhui Liu, Yang Zhang, Wei Liu, Chao Yan, Changyou |
| spellingShingle |
Tang, Xiaojiang Zhou, Yuhui Liu, Yang Zhang, Wei Liu, Chao Yan, Changyou Journal of Cellular Biochemistry Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer Cell Biology Molecular Biology Biochemistry |
| author_sort |
tang, xiaojiang |
| spelling |
Tang, Xiaojiang Zhou, Yuhui Liu, Yang Zhang, Wei Liu, Chao Yan, Changyou 0730-2312 1097-4644 Wiley Cell Biology Molecular Biology Biochemistry http://dx.doi.org/10.1002/jcb.29679 <jats:title>Abstract</jats:title><jats:p>As an aggressive breast cancer (BCa) subtype, triple‐negative breast cancer (TNBC) responses poorly to chemotherapy and endocrine therapy, and usually has a worse prognosis. This is largely due to the lack of specific therapeutic targets, laying claim to an imperious demand to clarify the key signaling pathways potentiating TNBC progression. Herein, we report that expression levels of the liver‐specific bHLH‐Zip transcription factor (LISCH7), a recently identified key player in cancerous progression, preferentially enriched in TNBC in comparison with other BCa subtypes, and this upregulation was observed to be correlated to a poor survival outcome in patients with TNBC. Ablation of LISCH7 in TNBC cells impaired cell proliferation, reduced cell invasiveness, and enhanced sensitivity to the first‐line chemotherapeutic drug docetaxel at both in vitro and in vivo levels. Importantly, concurrent induction of <jats:italic>TGFB1</jats:italic>, the gene encoding transforming growth factor‐β1 (TGF‐β1), an essential multipluripotent regulator of TNBC, was accompanied with these alterations in cancerous properties. We further showed that LISCH7 could directly bind to the <jats:italic>TGFB1</jats:italic> promoter and stimulate <jats:italic>TGFB1</jats:italic> transcription in TNBC cells. The recruitment of LISCH7 onto the <jats:italic>TGFB1</jats:italic> chromatin and transactivation of <jats:italic>TGFB1</jats:italic> were substantially augmented by treatment with the exogenous TGF‐β1 in a time‐ and dose‐dependent manner. Collectively, these findings suggest that LISCH7 and TGF‐β1 form a reciprocal positive regulatory loop and cooperatively regulate cancerous progression in TNBC cells. Thus, simultaneous inhibition of both LISCH7 and TGF‐β1 signaling may represent a more effective approach to counteract advanced TNBC.</jats:p> Potentiation of cancerous progression by LISCH7 via direct stimulation of <i>TGFB1</i> transcription in triple‐negative breast cancer Journal of Cellular Biochemistry |
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| title |
Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_unstemmed |
Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_full |
Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_fullStr |
Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_full_unstemmed |
Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_short |
Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_sort |
potentiation of cancerous progression by lisch7 via direct stimulation of <i>tgfb1</i> transcription in triple‐negative breast cancer |
| topic |
Cell Biology Molecular Biology Biochemistry |
| url |
http://dx.doi.org/10.1002/jcb.29679 |
| publishDate |
2020 |
| physical |
4642-4653 |
| description |
<jats:title>Abstract</jats:title><jats:p>As an aggressive breast cancer (BCa) subtype, triple‐negative breast cancer (TNBC) responses poorly to chemotherapy and endocrine therapy, and usually has a worse prognosis. This is largely due to the lack of specific therapeutic targets, laying claim to an imperious demand to clarify the key signaling pathways potentiating TNBC progression. Herein, we report that expression levels of the liver‐specific bHLH‐Zip transcription factor (LISCH7), a recently identified key player in cancerous progression, preferentially enriched in TNBC in comparison with other BCa subtypes, and this upregulation was observed to be correlated to a poor survival outcome in patients with TNBC. Ablation of LISCH7 in TNBC cells impaired cell proliferation, reduced cell invasiveness, and enhanced sensitivity to the first‐line chemotherapeutic drug docetaxel at both in vitro and in vivo levels. Importantly, concurrent induction of <jats:italic>TGFB1</jats:italic>, the gene encoding transforming growth factor‐β1 (TGF‐β1), an essential multipluripotent regulator of TNBC, was accompanied with these alterations in cancerous properties. We further showed that LISCH7 could directly bind to the <jats:italic>TGFB1</jats:italic> promoter and stimulate <jats:italic>TGFB1</jats:italic> transcription in TNBC cells. The recruitment of LISCH7 onto the <jats:italic>TGFB1</jats:italic> chromatin and transactivation of <jats:italic>TGFB1</jats:italic> were substantially augmented by treatment with the exogenous TGF‐β1 in a time‐ and dose‐dependent manner. Collectively, these findings suggest that LISCH7 and TGF‐β1 form a reciprocal positive regulatory loop and cooperatively regulate cancerous progression in TNBC cells. Thus, simultaneous inhibition of both LISCH7 and TGF‐β1 signaling may represent a more effective approach to counteract advanced TNBC.</jats:p> |
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| author | Tang, Xiaojiang, Zhou, Yuhui, Liu, Yang, Zhang, Wei, Liu, Chao, Yan, Changyou |
| author_facet | Tang, Xiaojiang, Zhou, Yuhui, Liu, Yang, Zhang, Wei, Liu, Chao, Yan, Changyou, Tang, Xiaojiang, Zhou, Yuhui, Liu, Yang, Zhang, Wei, Liu, Chao, Yan, Changyou |
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| description | <jats:title>Abstract</jats:title><jats:p>As an aggressive breast cancer (BCa) subtype, triple‐negative breast cancer (TNBC) responses poorly to chemotherapy and endocrine therapy, and usually has a worse prognosis. This is largely due to the lack of specific therapeutic targets, laying claim to an imperious demand to clarify the key signaling pathways potentiating TNBC progression. Herein, we report that expression levels of the liver‐specific bHLH‐Zip transcription factor (LISCH7), a recently identified key player in cancerous progression, preferentially enriched in TNBC in comparison with other BCa subtypes, and this upregulation was observed to be correlated to a poor survival outcome in patients with TNBC. Ablation of LISCH7 in TNBC cells impaired cell proliferation, reduced cell invasiveness, and enhanced sensitivity to the first‐line chemotherapeutic drug docetaxel at both in vitro and in vivo levels. Importantly, concurrent induction of <jats:italic>TGFB1</jats:italic>, the gene encoding transforming growth factor‐β1 (TGF‐β1), an essential multipluripotent regulator of TNBC, was accompanied with these alterations in cancerous properties. We further showed that LISCH7 could directly bind to the <jats:italic>TGFB1</jats:italic> promoter and stimulate <jats:italic>TGFB1</jats:italic> transcription in TNBC cells. The recruitment of LISCH7 onto the <jats:italic>TGFB1</jats:italic> chromatin and transactivation of <jats:italic>TGFB1</jats:italic> were substantially augmented by treatment with the exogenous TGF‐β1 in a time‐ and dose‐dependent manner. Collectively, these findings suggest that LISCH7 and TGF‐β1 form a reciprocal positive regulatory loop and cooperatively regulate cancerous progression in TNBC cells. Thus, simultaneous inhibition of both LISCH7 and TGF‐β1 signaling may represent a more effective approach to counteract advanced TNBC.</jats:p> |
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| spelling | Tang, Xiaojiang Zhou, Yuhui Liu, Yang Zhang, Wei Liu, Chao Yan, Changyou 0730-2312 1097-4644 Wiley Cell Biology Molecular Biology Biochemistry http://dx.doi.org/10.1002/jcb.29679 <jats:title>Abstract</jats:title><jats:p>As an aggressive breast cancer (BCa) subtype, triple‐negative breast cancer (TNBC) responses poorly to chemotherapy and endocrine therapy, and usually has a worse prognosis. This is largely due to the lack of specific therapeutic targets, laying claim to an imperious demand to clarify the key signaling pathways potentiating TNBC progression. Herein, we report that expression levels of the liver‐specific bHLH‐Zip transcription factor (LISCH7), a recently identified key player in cancerous progression, preferentially enriched in TNBC in comparison with other BCa subtypes, and this upregulation was observed to be correlated to a poor survival outcome in patients with TNBC. Ablation of LISCH7 in TNBC cells impaired cell proliferation, reduced cell invasiveness, and enhanced sensitivity to the first‐line chemotherapeutic drug docetaxel at both in vitro and in vivo levels. Importantly, concurrent induction of <jats:italic>TGFB1</jats:italic>, the gene encoding transforming growth factor‐β1 (TGF‐β1), an essential multipluripotent regulator of TNBC, was accompanied with these alterations in cancerous properties. We further showed that LISCH7 could directly bind to the <jats:italic>TGFB1</jats:italic> promoter and stimulate <jats:italic>TGFB1</jats:italic> transcription in TNBC cells. The recruitment of LISCH7 onto the <jats:italic>TGFB1</jats:italic> chromatin and transactivation of <jats:italic>TGFB1</jats:italic> were substantially augmented by treatment with the exogenous TGF‐β1 in a time‐ and dose‐dependent manner. Collectively, these findings suggest that LISCH7 and TGF‐β1 form a reciprocal positive regulatory loop and cooperatively regulate cancerous progression in TNBC cells. Thus, simultaneous inhibition of both LISCH7 and TGF‐β1 signaling may represent a more effective approach to counteract advanced TNBC.</jats:p> Potentiation of cancerous progression by LISCH7 via direct stimulation of <i>TGFB1</i> transcription in triple‐negative breast cancer Journal of Cellular Biochemistry |
| spellingShingle | Tang, Xiaojiang, Zhou, Yuhui, Liu, Yang, Zhang, Wei, Liu, Chao, Yan, Changyou, Journal of Cellular Biochemistry, Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer, Cell Biology, Molecular Biology, Biochemistry |
| title | Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_full | Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_fullStr | Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_full_unstemmed | Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_short | Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| title_sort | potentiation of cancerous progression by lisch7 via direct stimulation of <i>tgfb1</i> transcription in triple‐negative breast cancer |
| title_unstemmed | Potentiation of cancerous progression by LISCH7 via direct stimulation of TGFB1 transcription in triple‐negative breast cancer |
| topic | Cell Biology, Molecular Biology, Biochemistry |
| url | http://dx.doi.org/10.1002/jcb.29679 |