Correction: miR-200c inhibits TGF-β-induced-EMT to restore trastuzumab sensitivity by targeting ZEB1 and ZEB2 in gastric cancer

Zhou, Xinliang; Men, Xinyi; Zhao, Riyang; Han, Jing; Fan, Zhisong; Wang, Yudong; Lv, Yalei; Zuo, Jing; Zhao, Lianmei; Sang, Meixiang; Liu, Xiande; Shan, Baoen

doi:10.1038/s41417-020-00241-0

Cited by 4 publications

(4 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Many studies showed that EMT is a crucial step in the invasion and metastasis of malignant tumors [20]. Therefore, we hypothesized that GAL-1/LGALS1 promotes the invasion and metastasis of GC through EMT.…”

Section: Discussionmentioning

confidence: 95%

See 1 more Smart Citation

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition

You¹,

Wu²,

Zhao³

et al. 2021

Preprint

View full text Add to dashboard Cite

Background The gastric cancer (GC) microenvironment has important effects on biological behaviors, such as tumor cell invasion and metastasis. However, the mechanism by which the GC microenvironment promotes GC cell invasion and metastasis is unknown. The present study aimed to clarify the effects and mechanism of galectin-1 (GAL-1, encoded by LGALS1) on GC invasion and metastasis in the GC microenvironment.Methods The expression of GAL-1/ LGALS1 was determined using western blotting, immunohistochemistry, and quantitative real-time reverse transcription PCR in GC tissues. Besides, methods including stable transfection, Matrigel invasion and migration assays, and wound-healing assays in vitro; and metastasis assays in vivo, were also conducted.Results GAL-1 from cancer-associated fibroblasts (CAFs) induced the epithelial‑mesenchymal transition (EMT) of GC cells though the transforming growth factor beta (TGF-β1)/ Sma- and mad-related protein (Smad) pathway, and affected the prognosis of patients with GC. The level of GAL-1 was high in CAFs, and treating MGC-803 and SGC -7901 cell line with the conditioned medium from CAFs promoted their invasion and metastasis abilities. Overexpression of LGALS1 promoted the expression of TGF-β1 and induced EMT of GC cell lines. A TGF-β1 antagonist inhibited the invasion and migration of GC cells. In vivo, overexpression of LGALS1 promoted GC growth and metastasis, and the TGF-β1 antagonist dramatically reversed these events. Conclusions These findings suggested that high expression of GAL-1 in the GC microenvironment predicts a poor prognosis in patients with GC by promoting the migration and invasion of GC cells via EMT through the TGF-β1/Smad signaling pathway. The results might provide new therapeutic targets to treat GC.

show abstract

Section: Discussionmentioning

confidence: 95%

“…Numerous signaling pathways are involved in EMT through cooperation and antagonism, such as transforming growth factor beta (TGF-β), Wnt/beta-catenin, and Ras-mitogen activated protein kinase (MAPKl). [18][19][20]. TGF-β is considered the most important factor that induces EMT in developmental processes and other pathological states.…”

mentioning

confidence: 99%

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition

You¹,

Wu²,

Zhao³

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…For the invasion and metastasis of malignant tumors, EMT is a vital step [ 21 ], prompting us to hypothesize that GAL-1/ LGALS1 via EMT promotes GC invasion and metastasis. This hypothesis was tested by examining the EMT-related biomarkers Vimentin and E-Cadherin in GC and metastatic lymph nodes with IHC, which showed that the level of GAL-1 was related to EMT in GCT.…”

Section: Discussionmentioning

confidence: 99%

“…EMT induces loss of polarity in epithelial cells, thereby decreasing their contacts with stromal and peripheral cells, and reducing intercellular interactions, which enhance cell migration and motility. Numerous signaling pathways are involved in EMT through cooperation and antagonism, such as transforming growth factor beta (TGF-β), Wnt/beta-catenin, and Ras-mitogen activated protein kinase (MAPKl) [ 19 – 21 ]. TGF-β is an important EMT-inducing factor during developmental processes and pathological states.…”

Section: Introductionmentioning

confidence: 99%

Fibroblastic galectin-1-fostered invasion and metastasis are mediated by TGF-β1-induced epithelial-mesenchymal transition in gastric cancer

You

Zhao

et al. 2021

Aging

View full text Add to dashboard Cite

Background The gastric cancer (GC) microenvironment has important effects on biological behaviors, such as tumor cell invasion and metastasis. However, the mechanism by which the GC microenvironment promotes GC cell invasion and metastasis is unknown. The present study aimed to clarify the effects and mechanism of galectin-1 (GAL-1, encoded by LGALS1 ) on GC invasion and metastasis in the GC microenvironment. Methods The expression of GAL-1/ LGALS1 was determined using western blotting, immunohistochemistry, and quantitative real-time reverse transcription PCR in GC tissues. Besides, methods including stable transfection, Matrigel invasion and migration assays, and wound-healing assays in vitro ; and metastasis assays in vivo , were also conducted. Results GAL-1 from cancer-associated fibroblasts (CAFs) induced the epithelial-mesenchymal transition (EMT) of GC cells though the transforming growth factor beta (TGF-β1)/ Sma- and mad-related protein (Smad) pathway, and affected the prognosis of patients with GC. The level of GAL-1 was high in CAFs, and treating MGC-803 and SGC -7901 cell line with the conditioned medium from CAFs promoted their invasion and metastasis abilities. Overexpression of LGALS1 promoted the expression of TGF-β1 and induced EMT of GC cell lines. A TGF-β1 antagonist inhibited the invasion and migration of GC cells. In vivo , overexpression of LGALS1 promoted GC growth and metastasis, and the TGF-β1 antagonist dramatically reversed these events. Conclusions These findings suggested that high expression of GAL-1 in the GC microenvironment predicts a poor prognosis in patients with GC by promoting the migration and invasion of GC cells via EMT through the TGF-β1/Smad signaling pathway. The results might provide new therapeutic targets to treat GC.

show abstract

HER2-Directed Therapy in Advanced Gastric and Gastroesophageal Adenocarcinoma: Triumphs and Troubles

Grieb

Agarwal

2021

Curr. Treat. Options in Oncol.

View full text Add to dashboard Cite

Correction: miR-200c inhibits TGF-β-induced-EMT to restore trastuzumab sensitivity by targeting ZEB1 and ZEB2 in gastric cancer

Cited by 4 publications

References 0 publications

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition

Fibroblastic galectin-1-fostered invasion and metastasis are mediated by TGF-β1-induced epithelial-mesenchymal transition in gastric cancer

HER2-Directed Therapy in Advanced Gastric and Gastroesophageal Adenocarcinoma: Triumphs and Troubles

Contact Info

Product

Resources

About

Correction: miR-200c inhibits TGF-β-induced-EMT to restore trastuzumab sensitivity by targeting ZEB1 and ZEB2 in gastric cancer

Cited by 4 publications

References 0 publications

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through&nbsp;TGF-β1-Induced Epithelial-Mesenchymal Transition

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through&nbsp;TGF-β1-Induced Epithelial-Mesenchymal Transition

Fibroblastic galectin-1-fostered invasion and metastasis are mediated by TGF-β1-induced epithelial-mesenchymal transition in gastric cancer

HER2-Directed Therapy in Advanced Gastric and Gastroesophageal Adenocarcinoma: Triumphs and Troubles

Contact Info

Product

Resources

About

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition

Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition