Epithelial–mesenchymal transition and tumour invasion

Guarino, Marcello

doi:10.1016/j.biocel.2007.07.011

Cited by 332 publications

(281 citation statements)

References 26 publications

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“…HCC is associated with a high potential for vascular invasion, metastasis and recurrence even after surgical resection, leading to poor prognosis (Altekruse et al, 2012). An important biological process that has been shown to underlie tumor progression and metastasis is EMT (Guarino, 2007). Recently, it is widely accepted that EMT is the initiate step of intrahepatic and extra-hepatic (Maheswaran et al, 2012).…”

Section: Discussionmentioning

confidence: 99%

“…EMT describes the dedifferentiation switch between polarized epithelial cancer cells and contractile and motile mesenchymal (invasive) cells during cancer progression and metastasis (Guarino, 2007). We first examined EGFR expression in four HCC cell lines, including Bel-7402, MHC-97-H, SMMC-7721 and HepG2.…”

Section: Egf Promotes Emt and Cell Migration In Hcc Cell Linesmentioning

confidence: 99%

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PKM2 Regulates Hepatocellular Carcinoma Cell Epithelial-mesenchymal Transition and Migration upon EGFR Activation

Fan

Shen²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Pyruvate kinase isozyme type M2 (PKM2) was first found in hepatocellular carcinoma (HCC), and its expression has been thought to correlate with prognosis. A large number of studies have demonstrated that epithelial-mesenchymal transition (EMT) is a crucial event in hepatocellular carcinoma (HCC) and associated metastasis, resulting in enhanced malignancy of HCC. However, the roles of PKM2 in HCC EMT and metastasis remain largely unknown. The present study aimed to determine the effects of PKM2 in EGF-induced HCC EMT and elucidate the molecular mechanisms in vitro. Our results showed that EGF promoted EMT in HCC cell lines as evidenced by altered morphology, expression of EMT-associated markers, and enhanced invasion capacity. Furthermore, the present study also revealed that nuclear translocation of PKM2, which is regulated by the ERK pathway, regulated β-catenin-TCF/LEF-1 transcriptional activity and associated EMT in HCC cell lines. These discoveries provide evidence of novel roles of PKM2 in the progression of HCC and potential therapeutic target for advanced cases.

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Section: Discussionmentioning

confidence: 99%

Section: Egf Promotes Emt and Cell Migration In Hcc Cell Linesmentioning

confidence: 99%

PKM2 Regulates Hepatocellular Carcinoma Cell Epithelial-mesenchymal Transition and Migration upon EGFR Activation

Fan

Shen²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…During EMT cell-cell junctions dissolve, the cytoskeleton reorganizes, proliferation increases and a switch from E-cadherin to integrinmediated adhesion and degradation of the basement membrane occurs [15]. Normally the intact basement membrane prevents epithelial cells from contact with the interstitial space; exposure to the extracellular matrix and the growth factors contained there could promote and/or enhance EMT and tumor progression [16]. There is also increasing evidence that inflammation and EMT may be influential in tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

Heinrich

Walser

Krysan

et al. 2011

Cancer Microenvironment

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The inflammatory tumor microenvironment (TME) has many roles in tumor progression and metastasis, including creation of a hypoxic environment, increased angiogenesis and invasion, changes in expression of microRNAs (miRNAs) and an increase in a stem cell phenotype. Each of these has an impact on epithelial mesenchymal transition (EMT), particularly through the downregulation of E-cadherin. Here we review seminal work and recent findings linking the role of inflammation in the TME, EMT and lung cancer initiation, progression and metastasis.Finally, we discuss the potential of targeting aspects of inflammation and EMT in cancer prevention and treatment.

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“…The knockdown of Drosophila CG15072 (homologous to mammalian SIK3) resulted in impairment of the LKB1-regulated apicalbasal polarity in retinal photoreceptor cells (Amin et al, 2009), showing that this orthologue of SIK3 is probably one of mediators of the LKB1 effect on the cells. Since loss of the cell polarity is closely associated with development of the epithelial-mesenchymal transition of epithelial-derived cancer cells during tumor metastasis (Guarino, 2007), it may represent a key mechanism by which LKB1 and SIK3 are related to cancers. Here, we report that SIK3 is an ovarian TAA.…”

Section: Introductionmentioning

confidence: 99%

Identification of salt-inducible kinase 3 as a novel tumor antigen associated with tumorigenesis of ovarian cancer

et al. 2011

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Existence of humoral immunity has been previously demonstrated in malignant ascitic fluids. However, only a limited number of immunogenic tumor-associated antigens (TAAs) were identified, and few of which are associated with ovarian cancer. Here, we identified saltinducible kinase 3 (SIK3) as a TAA through screening of a random peptide library in the phage display system. Overexpression of SIK3 markedly promoted cell proliferation, attenuated p21 Waf/Cip1 and p27 Kip expressions in low-grade OVCAR3 cells, and permitted the cells to grow in mice. Decrease in SIK3 expression in high-grade SK-OV3 cells consistently demonstrated its tumorigenic potency by modulating the protein levels of cell cycle regulators. When the expressions of SIK3 and CA125 were compared in cancer tissues, immunohistochemical (IHC) studies indicated that cytoplasm-localized SIK3 was highly expressed in 55% of the ovarian cancer samples. In contrast, it was rarely detected in adenomyosis, leiomyoma and normal ovary tissues, showing its higher specificity (97%) to CA125 (65%) in ovarian cancer. Moreover, experiments using pharmacological inhibitors to block SIK3-induced p21 Waf/Cip1 expression revealed that activation of c-Src and phosphoinositide-3-kinase were critically required for its biological activity, suggesting that they are the downstream signaling mediators of SIK3. These data were further supported by IHC studies, showing coexpression of c-Src with SIK3 in 85% of the ovarian tumor samples stained positive for SIK3. Collectively, our findings indicate that SIK3 is a novel ovarian TAA. Overexpression of SIK3 promotes G1/S cell cycle progression, bestows survival advantages to cancer cells for growth and correlates the clinicopathological conditions of patients with ovarian cancer.

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Epithelial–mesenchymal transition and tumour invasion

Cited by 332 publications

References 26 publications

PKM2 Regulates Hepatocellular Carcinoma Cell Epithelial-mesenchymal Transition and Migration upon EGFR Activation

PKM2 Regulates Hepatocellular Carcinoma Cell Epithelial-mesenchymal Transition and Migration upon EGFR Activation

The Inflammatory Tumor Microenvironment, Epithelial Mesenchymal Transition and Lung Carcinogenesis

Identification of salt-inducible kinase 3 as a novel tumor antigen associated with tumorigenesis of ovarian cancer

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