TGF-β isoforms induce EMT independent migration of ovarian cancer cells

Gao, Jingfang; Zhu, Yingjun; Nilsson, Mikael; Sundfeldt, Karin

doi:10.1186/s12935-014-0072-1

Cited by 89 publications

(77 citation statements)

References 34 publications

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“…TGF-β is synthesized as an inactive form by various cells, such as epithelial, hematopoietic, and neuronal cells [9]. TGF-β super family signaling mediators are important regulators of diverse physiological and pathological events [10][11][12]. Several pathways, involving many downstream proteins, mediate the effects of TGF-β1.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: TGF-β Regulates Survivin to Affect Cell Cycle and the Expression of EGFR and MMP9 in Glioblastoma

et al. 2015

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Transforming growth factor beta (TGF-β) is suggestive of a molecular target for cancer therapy due to its involvement in cell cycle, differentiation, and morphogenesis. Meanwhile, survivin is identified as an apoptosis inhibitor and involved in tumorgenesis. Here, we aimed to investigate the potential associations between TGF-β and survivin in glioblastoma U87 cell line. Survivin small interfering RNA (siRNA), Western blotting, and cell cycle analysis were introduced to detect relevant proteins in TGF-β pathways. In this study, we observed a concentration- and time-dependent increase of survivin expression after treatment with TGF-β1. However, the kinase inhibitors U0126 and LY294002 inhibited the upregulation of survivin in comparison with DMSO. In addition, survivin siRNA effectively abrogated survivin expression in U87 cells, therefore affected cells' entry into the S phase of cell cycle, and then repressed the expression of epidermal growth factor receptor (EGFR) and matrix metalloproteinase 9 (MMP9) in comparison with non-transfection. In conclusion, the present study shows that TGF-β upregulates survivin expression via ERK and PI3K/AKT pathway, leading to glioblastoma cell cycle progression. Thus, the blockade of survivin will allow for the treatment of glioblastoma, partially attributing to the inhibition of EGFR and MMP9 expression.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: TGF-β Regulates Survivin to Affect Cell Cycle and the Expression of EGFR and MMP9 in Glioblastoma

et al. 2015

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“…Mammalian TGF isoforms (TGF-β1, TGF-β2 and TGF-β3) share 97% amino acid sequence identity and signal through activation of TGF-β receptors (28). TGF-β isoforms play major roles in tumourigenesis mediated by the EMT through regulating cell growth, migration, invasion and metastasis (28,37,38). Although pathway analyses should be mandatory to further identify the involvement PRMT5 in EMT process, our present results might suggest that PRMT5 partially participate in EMT programs through its coordinate expression with other EMT-inducing molecules in GC cells.…”

Section: Discussionmentioning

confidence: 99%

Protein arginine methyltransferase 5 is associated with malignant phenotype and peritoneal metastasis in gastric cancer

Kanda

Shimizu

Fujii

et al. 2016

International Journal of Oncology

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Abstract. Identification of novel gastric cancer (GC)-related molecules is necessary to improve management of patients with GC in both diagnostic and therapeutic aspects. The aim of the present study was to determine whether protein arginine methyltransferase 5 (PRMT5) acts as an oncogene in the progression of GC and whether it serves as a novel diagnostic marker and therapeutic target. We conducted global expression profiling of GC cell lines and RNA interference experiments to evaluate the effect of PRMT5 expression on the phenotype of GC cells. We analysed tissues of 179 patients with GC to assess the association of PRMT5 mRNA levels with clinicopathological factors. Differential expression of PRMT5 mRNA by GC cell lines correlated positively with the levels of GEMIN2, STAT3 and TGFB3. PRMT5 knockdown reduced the proliferation, invasion and migration of a GC cell line. PRMT5 mRNA levels were significantly higher in GC tissues than the corresponding adjacent normal tissues and were independent of tumour depth, differentiation and lymph node metastasis. High PRMT5 expression was an independent risk factor of positive peritoneal lavage cytology (odds ratio 3.90, P=0.003) and decreased survival. PRMT5 enhances the malignant phenotype of GC cell lines and its expression in gastric tissues may serve as a biomarker for patient stratification and a potential target of therapy.

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“…Since elucidating the underlying mechanisms of metastasis occurred during the progression of EOC will make significant contributions toward combating this disease, a number of studies have identified several crucial regulators in the EMT, such as miR-125a, the miR-200 family of microRNAs (miR-141, miR-200a, b, c, and miR-429), miR-34, miR-205, zinc finger E-box binding homeobox 1 (ZEB1) and zinc finger E-box binding homeobox 2 (ZEB2) [11][12][13][14][15]. Especially, the plasma miR-205 has been indicated as a biomarker for ovarian cancer detection that complement CA-125, and the upregulation of miR-205 has also been reported to promote the invasion and proliferation of ovarian cancer cells [16]; ZEB1 has been identified as an activator of EMT in EOC cells [17], and the regulatory effect of miR-205 on ZEB1 expression has been confirmed based on various cancer cells, including breast cancer cells and papillary urothelial tumors of the urinary bladder [18,19].…”

Section: Accepted Manuscriptmentioning

confidence: 99%