pERK activation in esophageal carcinomas: Clinicopathological associations

Tasioudi, Konstantia E.; Saetta, Angelica A.; Sakellariou, Stratigoula; Levidou, Georgia; Michalopoulos, Nikolaos V.; Theodorou, Dimitrios; Patsouris, Efstratios; Korkolopoulou, Penelope

doi:10.1016/j.prp.2012.05.009

Cited by 20 publications

(18 citation statements)

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“…In head and neck squamous carcinoma, the levels of activated ERK1/2 correlated with higher nodal status and a higher proliferation rate and were increased in tumour relapses [23]. Thus, in several cancers as well as in ESCC, ERK pathway activation is associated with tumorigenesis and tumor progression of esophageal squamous cell carcinoma [24]–[25].…”

Section: Discussionmentioning

confidence: 99%

Expression of SLP-2 Was Associated with Invasion of Esophageal Squamous Cell Carcinoma

et al. 2013

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IntroductionStomatin-like protein 2 (SLP-2), a member of the Stomatin superfamily, has been identified as an oncogenic-related protein and found to be up-regulated in multi-cancers. Nonetheless, the expression pattern and regulation of SLP-2 in human esophageal squamous cell carcinoma (ESCC) remain unexplored.MethodsImmunohistochemistry and immunofluorescence staining analysis were performed to show SLP-2 expression and location. RNAi method was used to inhibit specific protein expression. Transwell assay was done to investigate cells invasive capability. RT-PCR and Western blot analysis were used to detect mRNA and protein expression levels.ResultsImmunohistochemical analysis showed that up-regulation of SLP-2 was found in invasive front compared with cancer central tissue in ESCC. Inhibition of SLP-2 by SLP-2 siRNA can decrease ESCC cells invasive capability through MMP-2 dependent manner. Up-regulation of SLP-2 was effectively abrogated by the ERK1/2 inhibitors either PD98059 or U0126, but no effect was showed by the treatment of AKT inhibitors either LY294002 or MK-2206. So the regulation of SLP-2 was involved in activation of the MAPK/ERK pathway.ConclusionsWe found that PMA/EGF could induce the up-regulated expression of SLP-2 probably through activating ERK signalling. The current study suggests that SLP-2 may represent an important molecular hallmark that is clinically relevant to the invasion of ESCC.

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Section: Discussionmentioning

confidence: 99%

Expression of SLP-2 Was Associated with Invasion of Esophageal Squamous Cell Carcinoma

et al. 2013

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“…Similar pathologic characteristics with regard to ERK expression/activation have also been detected in digestive tract cancers. In esophageal carcinoma, increasing p-ERK nuclear and cytoplasmic expression was found to be significantly correlated with tumor grade [97]. Likewise, high nuclear p-ERK expression in colorectal cancer was associated with highly invasive disease [98].…”

Section: Leptin Biology and Molecules Of Relevant Signal Transductmentioning

confidence: 99%

The potential role of leptin in tumor invasion and metastasis

Ray

Cleary

2017

Cytokine & Growth Factor Reviews

109

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The adipocyte-released hormone-like cytokine/adipokine leptin behaves differently in obesity compared to its functions in the normal healthy state. In obese individuals, elevated leptin levels act as a pro-inflammatory adipokine and are associated with certain types of cancers. Further, a growing body of evidence suggests that higher circulating leptin concentrations and/or elevated expression of leptin receptors (Ob-R) in tumors may be poor prognostic factors. Although the underlying pathological mechanisms of leptin’s association with poor prognosis are not clear, leptin can impact the tumor microenvironment in several ways. For example, leptin is associated with a number of biological components that could lead to tumor cell invasion and distant metastasis. This includes interactions with carcinoma-associated fibroblasts, tumor promoting effects of infiltrating macrophages, activation of matrix metalloproteinases, transforming growth factor-β signaling, etc. Recent studies also have shown that leptin plays a role in the epithelial-mesenchymal transition, an important phenomenon for cancer cell migration and/or metastasis. Furthermore, leptin’s potentiating effects on insulin-like growth factor-I, epidermal growth factor receptor and HER2/neu have been reported. Regarding unfavorable prognosis, leptin has been shown to influence both adenocarcinomas and squamous cell carcinomas. Features of poor prognosis such as tumor invasion, lymph node involvement and distant metastasis have been recorded in several cancer types with higher levels of leptin and/or Ob-R. This review will describe the current scenario in a precise manner. In general, obesity indicates poor prognosis in cancer patients.

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“…They play an important role in regulating cell survival, cell cycle, angiogenesis, metastasis, and metabolism . Several studies have demonstrated that the PI3K/Akt and MAPK/ERK signaling pathways are activated in the progression of ESCC . Additionally, FGFR4 overexpression can promote cell malignant growth, migration, invasion, and suppress apoptosis via the PI3K/Akt and MAPK/ERK pathways in colorectal cancer, rhabdomyosarcoma and ovarian cancer .…”

Section: Discussionmentioning

confidence: 99%

“…[40][41][42] Several studies have demonstrated that the PI3K/Akt and MAPK/ERK signaling pathways are activated in the progression of ESCC. 43,44 Additionally, FGFR4 overexpression can promote cell malignant growth, migration, invasion, and suppress apoptosis via the PI3K/ Akt and MAPK/ERK pathways in colorectal cancer, 38 rhabdomyosarcoma 45 and ovarian cancer. 31 In this study, we found that blocking FGFR4 could significantly inhibit its phosphorylation and further reduce the levels of phosphorylated AKT and ERK.…”

Section: Discussionmentioning

confidence: 99%

Blocking FGFR4 exerts distinct anti‐tumorigenic effects in esophageal squamous cell carcinoma

et al. 2018

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BackgroundThe FGFR family can be activated by FGFs and plays important roles in regulating cell growth, differentiation, migration, and angiogenesis. Recent studies have suggested that FGFR4 could regulate several processes, including tumor progression. Esophageal squamous cell carcinoma (ESCC) is a malignancy with high global occurrence. However, the molecule mechanism and the potential roles of FGFR4 in ESCC remain unknown.MethodsImmunohistochemistry and Western blotting were used to detect FGFR4 expression in ESCC samples and cell lines. Cell counting kit‐8, and clonogenic, transwell, flow cytometric, and tumor xenograft in nude mice assays were utilized to determine the effect of blocking FGFR4 in proliferation, invasion, migration, and apoptosis of ESCC cells.ResultsFGFR4 is frequently overexpressed in ESCC tissue and cell lines. in vitro assays have shown that blocking FGFR4 by a specific blocker, H3B‐6527, significantly decreases proliferation, invasion, and migration, and alters epithelial‐mesenchymal transition markers in ESCC cells. In addition, FGFR4 blockade is associated with the induction of apoptosis and affects PI3K/Akt and MAPK/ERK pathways. Moreover, FGFR4 blockade could significantly inhibit the growth of xenograft tumors in vivo.ConclusionOur findings suggest that blocking FGFR4 significantly suppresses the malignant behaviors of ESCC and indicate that FGFR4 is a potential target for the treatment of ESCC.

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pERK activation in esophageal carcinomas: Clinicopathological associations

Cited by 20 publications

References 28 publications

Expression of SLP-2 Was Associated with Invasion of Esophageal Squamous Cell Carcinoma

Expression of SLP-2 Was Associated with Invasion of Esophageal Squamous Cell Carcinoma

The potential role of leptin in tumor invasion and metastasis

Blocking FGFR4 exerts distinct anti‐tumorigenic effects in esophageal squamous cell carcinoma

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