Correlations of TNM staging and lymph node metastasis of gastric cancer with MRI features and VEGF expression

Pang, Lan; Wang, Jing; Fan, Yong; Xu, Rui; Bai, Yuping; Bai, Liangcai

doi:10.3233/cbm-181287

Cited by 27 publications

(27 citation statements)

References 17 publications

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“…In this study, ETAR overexpression was also associated with reduced survival time as determined by univariate and multivariate analyses. Similarly, and consistent with previous studies, age, tumor size, depth of invasion, lymph node and distant metastasis, and VEGF expression were all significantly associated with poor prognosis of gastric cancer patients . Our findings are also in agreement with earlier reports that correlated elevated expression of ETAR with the progression and poor prognosis in many tumors .…”

Section: Discussionsupporting

confidence: 93%

Endothelin‐A receptor in gastric cancer and enhanced antitumor activity of trastuzumab in combination with the endothelin‐A receptor antagonist ZD4054

Shen

et al. 2019

Annals of the New York Academy of Sciences

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Endothelin‐A receptor (ETAR) is overexpressed in cancers and can function through transactivation of the epidermal growth factor receptor. We explored ETAR in gastric cancer and investigated the antitumor effect of trastuzumab in combination with the ETAR antagonist ZD4054. The expression of ETAR was significantly correlated with the expression of vascular endothelial growth factor. Univariate and multivariate analyses further showed that ETAR expression correlated with reduced survival in gastric cancer patients. In vitro, ZD4054 increased the antiproliferative effect of trastuzumab in gastric cancer cell lines. Moreover, the addition of ZD4054 to trastuzumab significantly increased apoptosis in gastric cancer cell lines. In vivo, tumor growth was considerably inhibited by treatment with ZD4054 and trastuzumab, and the tumor volume in the trastuzumab and ZD4054 combination group was smaller than in the other groups. The detection of ETAR could help predict the prognosis of gastric cancer patients. Additionally, this study provides support for the therapeutic use of the combination of ZD4054 and trastuzumab as an anticancer treatment, especially for gastric cancer.

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Section: Discussionsupporting

confidence: 93%

Endothelin‐A receptor in gastric cancer and enhanced antitumor activity of trastuzumab in combination with the endothelin‐A receptor antagonist ZD4054

Shen

et al. 2019

Annals of the New York Academy of Sciences

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“…a-c qRT-PCR and western blotting analysis results showed that MCU expression was silenced by two MCU-siRNAs in HCT-116 and SW-480 cells. d Representative immunofluorescence images showing HIF-1α expression in HCTmetastasis, and clinical pathological prognosis (Pang et al 2018). Previous research found that knockdown of Piezo1 attenuated migration of human umbilical vein endothelial cells towards VEGF (Li et al 2014).…”

Section: Discussionmentioning

confidence: 97%

The function of Piezo1 in colon cancer metastasis and its potential regulatory mechanism

Sun

Liu

et al. 2020

J Cancer Res Clin Oncol

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Objective Increasing evidence has revealed that mechanical stress and elevated mechanical signals promote malignant tumor transformation and metastasis. This study aimed to explore the function of the mechanically activated ion-channel Piezo1 in the colon cancer metastasis and its potential regulatory mechanism. Methods First, we examined the expression levels of Piezo1 and mitochondrial calcium uniporter (MCU) both in colon cancer tissues and assessed the prognostic value of Piezo1 and MCU in a colon cancer cohort (n = 110). Second, functional assays were performed to investigate the effects of Piezo1 and MCU on colon cancer cell migration, invasion, and mitochondrial membrane potential. Third, we analyzed the expression of Piezo1, MCU, and HIF-1α by overexpressing/silencing each other's expression. Results We found that Piezo1 was up-regulated and MCU was down-regulated in colon cancer tissues. Piezo1 and MCU were both correlated with poor prognosis of patients with colon cancer. Overexpressing Piezo1 and silencing MCU could promote colon cancer cell migration and metastasis, reduce mitochondrial membrane potential, and promote each other's expression. We also found that HIF-1α was up-regulated in colon cancer tissues. Additionally, silencing Piezo1 inhibited the expression of HIF-1α and VEGF, which was contrary to MCU silencing. Intriguingly, Piezo1-overexpressing cells did not regain their migration behaviors when HIF-1α expression was inhibited, which was accompanied with the re-expression of MCU and VEGF. Conclusion In our study, Piezo1 is involved in colon cancer cell metastasis. Furthermore, our findings indicated a possible Piezo1-MCU-HIF-1α-VEGF axis, which still need further exploration.Keywords Colon cancer · Metastasis · Piezo1 · Mitochondrial calcium uniporter · HIF-1α Yanhua Sun and Ming Li have contributed equally to this work.

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“…Li et al 37 reported that VEGF expression led to colon cancer metastasis. In addition, in gastric cancer, VEGF expression is also correlated with TNM staging and lymph node metastasis 38 . Moreover, distant metastasis and poor prognosis are related to VEGF in osteosarcoma, ovarian cancer and breast cancer 39 - 41 .…”

Section: Discussionmentioning

confidence: 99%

VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma

et al. 2020

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Background: Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. Accumulating data have indicated that VEGF is involved in tumour metastasis. However, the mechanism through which VEGF regulates nasopharyngeal carcinoma (NPC) metastasis is largely unknown. This study aimed to examine the biological function of VEGF in NPC metastasis and its underlying mechanism. Methods: We used western blotting and qPCR to examine the difference in VEGF expression between NPC cells and the immortalized nasopharyngeal epithelial cell line NP69. Wound healing assays, transwell assays and animal experiments were used to further verify the role of VEGF in the invasion and migration of NPC cells. The protein levels of the epithelial-mesenchymal transition (EMT) and matrix metalloproteinase (MMP) family were analysed by immunofluorescence (IF) and western blotting. Enzyme-linked immunosorbent assay (ELISA) and transwell assays were used to determine whether VEGF enhanced the invasion and migration of NPC cells in an autocrine manner. Western blotting was used to examine how autocrine VEGF-VEGFR2 signalling regulated EMT and MMPs. Results: We observed higher levels of VEGF in NPC cells than that in NP69 cells and identified an association between high VEGF levels and tumour invasion and migration. Mechanistically, the VEGF-mediated increase in EMT markers, MMP2 and MMP9 promoted NPC cell invasion and migration. Additionally, NPC cells secreted VEGF to promote cell invasion, migration and angiogenesis. Autocrine VEGF-VEGFR2 signalling increased ERK1/2 phosphorylation, promoted EMT process and MMPs at the indicated times. Conclusion: This study revealed that VEGF plays a role in controlling NPC cell metastasis by regulating EMT markers and MMPs in an autocrine manner.

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Correlations of TNM staging and lymph node metastasis of gastric cancer with MRI features and VEGF expression

Cited by 27 publications

References 17 publications

Endothelin‐A receptor in gastric cancer and enhanced antitumor activity of trastuzumab in combination with the endothelin‐A receptor antagonist ZD4054

Endothelin‐A receptor in gastric cancer and enhanced antitumor activity of trastuzumab in combination with the endothelin‐A receptor antagonist ZD4054

The function of Piezo1 in colon cancer metastasis and its potential regulatory mechanism

VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma

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