Twist expression associated with the epithelial-mesenchymal transition in gastric cancer

Gong

Molecular Medicine Reports

et al. 2014

Abstract. The present study aimed to investigate the expression of interleukin-6 (IL-6) in gallbladder cancer (GBC) tissues and its correlation with survival rate. The association between IL-6 and epithelial-mesenchymal transition (EMT)-associated markers was also examined. Using immunohistochemistry, reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis, the protein and mRNA expression levels of IL-6, Twist, E-cadherin and Vimentin in 20 GBC tissues were analyzed. The IL-6, Twist and Vimentin proteins were overexpressed in 40, 20 and 70% of the human GBC samples, respectively. The protein expression of E-cadherin was higher in only 5% of the GBC samples. These differences were significant (P<0.05). Western blot analysis also revealed overexpression of IL-6, Twist and Vimentin and underexpression of E-cadherin in the GBC samples with poor differentiation, local invasion and a higher tumor-node-metastasis (TNM) stage (P<0.05). Higher mRNA expression levels of IL-6, Twist and Vimentin and a reduced expression level of E-cadherin were also demonstrated in the GBC tissues (P<0.05). The degree of differentiation, local invasion, lymph node metastasis and clinical stage were significantly associated with the mRNA expression levels of IL-6, Twist and E-cadherin. The increased expression levels of IL-6 and Twist and the reduced expression of E-cadherin correlated with shorter median survival rates (P<0.05). Line regression results revealed correlation among the mRNA expression levels of IL-6, Twist, E-cadherin and Vimentin. To the best of our knowledge, the present study is the first to demonstrate that IL-6 is associated with EMT-associated markers, tumor differentiation, local invasion, TNM stage and survival rates in GBC.

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression of interleukin-6 is associated with epithelial-mesenchymal transition and survival rates in gallbladder cancer

Gong

Molecular Medicine Reports

et al. 2014

International Journal of Oncology

“…A series of experiments have illustrated the considerable function of Twist as an oncogene in vivo, suggestive of its potency to be a target for the treatment of gastric carcinoma. Liu et al (29) discovered that Twist is expressed much higher in gastric cancer tissues compared to adjacent normal tissues at mRNA and protein levels by means of RT-PCR and western blotting. Likewise, abnormal Twist expression related strongly to lower 5-year survival rates in patients of GC in the Ru et al study, yet, they emphasized that the significance disappears in cases of stage IV (30).…”

Section: Epithelial-mesenchymal Transition and Gastric Cancermentioning

confidence: 99%

Interaction between Wnt/β-catenin pathway and microRNAs regulates epithelial-mesenchymal transition in gastric cancer (Review)

Zhuang

Jiang

et al. 2016

Abstract. Gastric cancer (GC) is the third primary cause of cancer-related mortality and one of the most common type of malignant diseases worldwide. Despite remarkable progress in multimodality therapy, advanced GC with high aggressiveness always ends in treatment failure. Epithelialmesenchymal transition (EMT) has been widely recognized to be a key process associating with GC evolution, during which cancer cells go through phenotypic variations and acquire the capability of migration and invasion. Wnt/β-catenin pathway has established itself as an EMT regulative signaling due to its maintenance of epithelial integrity as well as tight adherens junctions while mutations of its components will lead to GC initiation and diffusion. The E-cadherin/β-catenin complex plays an important role in stabilizing β-catenin at cell membrane while disruption of this compound gives rise to nuclear translocation of β-catenin, which accounts for upregulation of EMT biomarkers and unfavorable prognosis. Additionally, several microRNAs positively or negatively modify EMT by reciprocally acting with certain target genes of Wnt/β-catenin pathway in GC. Thus, this review centers on the strong associations between Wnt/β-catenin pathway and microRNAs during alteration of EMT in GC, which may induce advantageous therapeutic strategies for human gastric cancer.

“…It is regarded as a proto-oncogene and its role in inducing EMT has been widely studied in many in vitro and in vivo models. Overexpression of TWIST1 induces EMT in breast, pancreatic and gastric cancers [81][82][83]. In prostate cancer, TWIST1 has been shown to induce EMT by increasing N-cadherin and fibronectin expression, promoting a more mesenchymal phenotype associated with increased prostate cancer cell migration and invasion [84,85].…”

Section: Emt and Prostate Cancer Progressionmentioning

confidence: 99%

The Role of the IGF Axis in Epithelial-to-Mesenchymal Transition during the Progression of Prostate Cancer

Mansor¹,

Bahl²,

Holly³

et al. 2015

J. Anal. Oncol.

Prostate cancer is the second most common lethal cancer in men worldwide. Despite the fact that the prognosis for patients with localized disease is good, many patients succumb to metastatic disease with the development of resistance to hormone treatments. This is normally termed castration-resistant prostate cancer (CRPC). The development of metastatic, castration-resistant prostate cancer has been associated with epithelial-to-mesenchymal transition (EMT), a process where cancer cells acquire a more mesenchymal phenotype with enhanced migratory potential, invasiveness and elevated resistance to apoptosis. The main event in EMT is the repression of epithelial markers such as E-cadherin and upregulation of mesenchymal markers such as N-cadherin, vimentin and fibronectin. The insulin-like growth factor (IGF) signalling axis is essential for normal development and maintenance of tissues, including that of the prostate, and dysregulation of this pathway contributes to prostate cancer progression and malignant transformation. It is becoming increasingly clear that one of the ways in which the IGF axis impacts upon cancer progression is through promoting EMT. This review will explore the role of EMT in prostate cancer progression with a specific focus on the involvement of the IGF axis and its downstream signalling pathways in regulating EMT in prostate cancer.Keywords: Epithelial-to-mesenchymal transition, insulin-like growth factor family, prostate cancer progression, lifestyle factors. PROSTATE CANCERProstate cancer is the second most common lethal cancer diagnosed in men. According to The American Cancer Society, it is estimated that more than 220 000 new cases of prostate cancer will occur in the United States during 2015 accounting for about 26% of all cancers in men with a mortality rate of 9%: the second highest cause of cancer deaths in men after lung cancer [1].Age is the biggest risk factor for PCa with the incidence of prostate cancer being higher in older men particularly in men aged 65 and above [2]. The incidence of, and mortality from, prostate cancer varies hugely within different racial and ethnic groups. Much higher incidence and death rates are reported in black men compared to other races [3,4]: the reasons underlying these observations are still unclear but both genetic and/or environmental influences may be involved. A number of epidemiology studies have also reported that family history is a risk factor for PCa-with approximately 5-10% of cases being attributable to inherited genetic factors or PCa susceptibility genes [5,6] The prognosis for patients with localized disease is good, however the morbidity and mortality for prostate cancer patients who develop metastatic disease is high [7]. Androgen deprivation therapy (ADT) which involves surgical or chemical castration plays an important role in the treatment and management of prostate cancer and is also utilised as an adjuvant or neo-adjuvant treatment for high-risk disease [8]. The response to the treatments is however temporary a...