Transforming Growth Factor β1 Promotes Migration and Invasion of Human Hepatocellular Carcinoma Cells Via Up-Regulation of Connective Tissue Growth Factor

Liu, Haizhou; Wang, Shaoyang; Ma, Weimin; Lu, You‐Guang

doi:10.1007/s12013-015-0693-6

Cited by 7 publications

(7 citation statements)

References 33 publications

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“…It was known that ACL had poor healing capacity, with a substantially high rate of failure (40–100%), even after surgical repair using suture (Strand et al, 2005, Taylor et al, 2015). The reconstruction of ACL has remained the gold standard of care for ACL injuries, especially for young individuals and some athletes who aim to return to high-level sporting activities (Liu et al, 2015a, Musahl et al, 2011). However, for now though, surgical treatment of ACL injury is costly, with variable outcomes (Wang et al, 2015, Kiapour et al, 2014), which are often not successful at returning patients to their pre-injury activity level (Ardern et al, 2011, Zaheer et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: The influence of connective tissue growth factor on rabbit ligament injury repair

Zhang

Zheng

Chen

et al. 2017

Saudi Pharmaceutical Journal

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Section: Introductionmentioning

confidence: 99%

RETRACTED: The influence of connective tissue growth factor on rabbit ligament injury repair

Zhang

Zheng

Chen

et al. 2017

Saudi Pharmaceutical Journal

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“…Liver histology revealed disrupted lobular architecture, bridging fibrosis, and necro-inflammatory liver damage. Liver fibrogenesis was confirmed by the increased deposition of collagen and the increased expression of α-Sma , a specific marker of hepatic stellate cell activation, 42 in addition to the upregulation of Tgf-β and Ctgf pro-fibrotic molecules 43, 44. The neoplastic nature of the hepatocellular nodules was confirmed by histology, which identified a spectrum of lesions ranging from dysplastic foci or nodules to HCC.…”

Section: Discussionmentioning

confidence: 96%

MicroRNA-Based Prophylaxis in a Mouse Model of Cirrhosis and Liver Cancer

Callegari

Domenicali

Shankaraiah

et al. 2019

Molecular Therapy - Nucleic Acids

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Most hepatocellular carcinomas (HCCs) arise in the context of chronic liver disease and/or cirrhosis. Thus, chemoprevention in individuals at risk represents an important but yet unproven approach. In this study, we investigated the ability of microRNA (miRNA)-based molecules to prevent liver cancer development in a cirrhotic model. To this end, we developed a mouse model able to recapitulate the natural progression from fibrosis to HCC, and then we tested the prophylactic activity of an miRNA-based approach in the model. The experiments were carried out in the TG221 transgenic mouse, characterized by the overexpression of miR-221 in the liver and predisposed to the development of liver tumors. TG221 as well as wild-type mice were exposed to the hepatotoxin carbon tetrachloride (CCl4) to induce chronic liver damage. All mice developed liver cirrhosis, but only TG221 mice developed nodular lesions in 100% of cases within 6 months of age. The spectrum of lesions ranged from dysplastic foci to carcinomas. To investigate miRNA-based prophylactic approaches, anti-miR-221 oligonucleotides or miR-199a-3p mimics were administered to TG221 CCl4-treated mice. Compared to control animals, a significant reduction in number, size, and, most significantly, malignant phenotype of liver nodules was observed, thus demonstrating an important prophylactic action of miRNA-based molecules. In summary, in this article, we not only report a simple model of liver cancer in a cirrhotic background but also provide evidence for a potential miRNA-based approach to reduce the risk of HCC development.

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“…The evidences showed that the TGFβ1 participated in tumorigenesis, development and metastasis 30. The high level of TGFβ1 was associated with poor postoperative metastasis in colorectal cancer 31.…”

Section: Discussionmentioning

confidence: 99%

<p>TGFβ1 is essential for MSCs-CAFs differentiation and promotes HCT116 cells migration and invasion via JAK/STAT3 signaling</p>

Tan¹,

Cao²,

He³

et al. 2019

OTT

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Background and purpose Colorectal cancer (CRC) frequently metastasizes to the liver, which involves the participation of multiple cytokines. Tumor microenvironment (TME) composed of cancer-associated fibroblasts (CAFs) and tumor cells acts as an essential factor in cancer metastasis. Transforming growth factor β1 (TGFβ1) is a vital cytokine involved in migration and invasion of cancer cells. However, the underlying mechanisms remain unclear. In the present study, we aimed to investigate the role and molecular mechanisms of TGFβ1 in TME. Methods The conditioned medium prepared from colorectal cancer HCT116 and HT29 cells was used to culture mesenchymal stem cells (MSCs). The differentiation of MSCs to CAFs was detected by flow cytometry. The role of TGFβ1 in colorectal cancer cells metastasis was examined by wound-healing assay and transwell assay. And the activation of the Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) signaling pathway was measured by Western blot assay. Results TGFβ1 induced the differentiation of MSCs to CAFs and improved HCT116 and HT29 cells migration and invasion. Meanwhile, TGFβ1 also upregulated the phosphorylation of STAT3 and enhanced the nuclear localization of p-STAT3, which activated JAK/STAT3 signaling pathway. Conclusion TGFβ1 induced the differentiation of MSCs into CAFs and promoted the migration and invasion of HCT116 and HT29 cells, which depended on the activation of JAK/STAT3 signaling pathway.

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Transforming Growth Factor β1 Promotes Migration and Invasion of Human Hepatocellular Carcinoma Cells Via Up-Regulation of Connective Tissue Growth Factor

Cited by 7 publications

References 33 publications

RETRACTED: The influence of connective tissue growth factor on rabbit ligament injury repair

RETRACTED: The influence of connective tissue growth factor on rabbit ligament injury repair

MicroRNA-Based Prophylaxis in a Mouse Model of Cirrhosis and Liver Cancer

<p>TGFβ1 is essential for MSCs-CAFs differentiation and promotes HCT116 cells migration and invasion via JAK/STAT3 signaling</p>

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