2019
DOI: 10.1186/s13046-019-1298-5
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Correction to: Calycosin suppresses TGF-β-induced epithelial-to-mesenchymal transition and migration by upregulating BATF2 to target PAI-1 via the Wnt and PI3K/Akt signaling pathways in colorectal cancer cells

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Cited by 4 publications
(4 citation statements)
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“…TGF-β is involved in regulating the biological function of malignant tumors through several pathways, including the Jagged1/Notch, Wnt, JAK2/STAT3, and PI3K/AKT/mTOR signaling pathways [13][14][15][16]. Moreover, regulation of Akt/ mTOR pathway activity can inhibit osteosarcoma cell proliferation, arrest the cell cycle, induce apoptosis, and suppress invasion and metastasis, suggesting the involvement of this pathway in the development of osteosarcoma [17][18][19][20].…”
Section: Introductionmentioning
confidence: 99%
“…TGF-β is involved in regulating the biological function of malignant tumors through several pathways, including the Jagged1/Notch, Wnt, JAK2/STAT3, and PI3K/AKT/mTOR signaling pathways [13][14][15][16]. Moreover, regulation of Akt/ mTOR pathway activity can inhibit osteosarcoma cell proliferation, arrest the cell cycle, induce apoptosis, and suppress invasion and metastasis, suggesting the involvement of this pathway in the development of osteosarcoma [17][18][19][20].…”
Section: Introductionmentioning
confidence: 99%
“…However, cotreatment of HT-29 with IGF-1 could recover calycosin-induced cell autophagy. Wang found that calycosin inhibited colorectal cancer proliferation and migration by enhancing BATF2 to target plasminogen activator inhibitor-1 [ 27 ]. Moreover, this molecule was able to abolish transforming growth factor ß - (TGF- β -) induced epithelial-to-mesenchymal transition via altering Wnt mechanism [ 27 ].…”
Section: Pharmacological Activities Of Calycosinmentioning
confidence: 99%
“…Wang found that calycosin inhibited colorectal cancer proliferation and migration by enhancing BATF2 to target plasminogen activator inhibitor-1 [ 27 ]. Moreover, this molecule was able to abolish transforming growth factor ß - (TGF- β -) induced epithelial-to-mesenchymal transition via altering Wnt mechanism [ 27 ]. In addition, calycosin robustly restricted HCT-116 cells viability and invasiveness by enhancing ER β and phosphatase and tensin homolog (PTEN) expressions [ 28 ].…”
Section: Pharmacological Activities Of Calycosinmentioning
confidence: 99%
“…Another cytokine, transforming growth factor -beta (TGF-β), a superfamily regulates tissue regeneration can also induce epithelial-mesenchymal transition (EMT) [12,13]. TGF-β might increase the levels of PAI-1 [14,15]. Therefore, we designed the prospected study including testing PAI-1, t-PA, TGF-β and Interferon-gamma (IFN-γ) in pleural effusion then observing the pleural changes during the chemotherapy, trying to find out the underlying predictive risk factors of PTM occurrence.…”
Section: Introductionmentioning
confidence: 99%