CD31 regulates metastasis by inducing epithelial–mesenchymal transition in hepatocellular carcinoma via the ITGB1-FAK-Akt signaling pathway

Zhang, Xu Dong; Kong, Ling Qun; Zhu, Xiao Dong; Cai, Hao; Wang, Chenghao; Shi, Wen; Cao, Man Qing; Li, Xiayu; Li, Kang Shuai; Zhang, Shizhe; Chai, Zong Tao; Ao, Jian; Ye, Bo Gen; Sun, Hui‐Chuan

doi:10.1016/j.canlet.2018.05.004

Cited by 80 publications

(71 citation statements)

References 51 publications

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“…Furthermore, we also found that the expression of CD31 decreased after VEGF was silenced ( Figure 6E and F, all P<0.001). As a vascular marker, CD31 is not only related to vascular density but can also induce tumour metastasis [27][28][29][30]. In the lung metastasis model, we found that the number of lung metastatic nodules in the shRNA group was significantly lower than that in the NC group ( Figure 6C and D, P<0.01).…”

Section: Vegf Promotes Npc Tumour Growth and Metastasis In Vivomentioning

confidence: 88%

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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Section: Vegf Promotes Npc Tumour Growth and Metastasis In Vivomentioning

confidence: 88%

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

et al. 2020

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“…Overexpression of vimentin and N-cadherin contributes to increased cell motility; as a result, these cells easily spread to distant or surrounding tissues (Liu et al, 2015;Loh et al, 2019;Rai and Ahmed, 2019). In liver cancer, studies have found that EMT activation induces liver fibrogenesis and carcinogenesis (Pinzani, 2011) and also promotes the invasion and migration of liver cancer cells (Peng et al, 2018;Zhang et al, 2018). In the present study, the investigation of underlying mechanisms revealed that lnc-GNAT1-1 exerted regulatory effects by modulating the EMT process in liver cancer cells.…”

Section: Discussionmentioning

confidence: 51%

Long Non-coding RNA lnc-GNAT1-1 Suppresses Liver Cancer Progression via Modulation of Epithelial–Mesenchymal Transition

Wang

Tang

et al. 2020

Front. Genet.

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Recent studies have investigated the modulatory roles of long non-coding RNAs in the onset and progression of liver cancer. The present study aimed to elucidate the role of lnc-GNAT1-1 in liver cancer development and to explore the underlying mechanisms. Quantitative real-time polymerase chain reaction was performed to measure the expression levels of lnc-GNAT1-1 in cancerous tissues from patients with liver cancer and in liver cancer cell lines. The proliferative ability and apoptotic rates of liver cancer cells were measured using the counting kit-8 (CCK-8), colony formation, and flow cytometry assays. The abilities to invade and migrate were measured using Transwell assays. Epithelial-mesenchymal transition (EMT)-related proteins, E-cadherin, N-cadherin, and vimentin, were measured using western blotting. A nude mouse model was injected with xenografts to evaluate tumor growth in vivo. Downregulation of lnc-GNAT1-1 was observed in cancerous tissues from patients with liver cancer and in liver cancer cell lines, and low expression levels of lnc-GNAT1-1 were related to advanced TNM stage. Lnc-GNAT1-1 knockdown promoted invasion, migration, and proliferation of liver cancer cells and inhibited apoptosis, while lnc-GNAT1-1 upregulation exerted the opposite effects. The expression levels of lnc-GNAT1-1 negatively correlated with in vivo tumor growth in a xenograft nude mouse model. Mechanistic experiments revealed that lnc-GNAT1-1 exerted anti-tumor effects in liver cancer cells by inhibiting EMT. In conclusion, this study suggests that lnc-GNAT1-1 suppresses liver cancer progression by modulating EMT.

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“…CD31 (platelet endothelial cell adhesion molecule-1, PECAM-1) is expressed in blood vessels and lymphatic endothelial cells and involved in tumor angiogenesis and metastasis (20,21). The combination group showed weaker CD31 expression compared to single therapy.…”

Section: Discussionmentioning

confidence: 99%

Combination Therapy of Prostate Cancer by Oncolytic Adenovirus Harboring Interleukin 24 and Ionizing Radiation

Mao¹,

Kan

et al. 2020

Front. Oncol.

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Prostate cancer is a common malignant tumor and the second leading cause of cancer-related death in men. Radiation therapy is a curative treatment for localized prostate cancer and has a limited effect for castration-resistant prostate cancer (CRPC). Interleukin 24 (IL-24) has a radiosensitizing effect in cancer cells. Our previous studies showed that ZD55-IL-24, an oncolytic adenovirus harboring IL-24, had better anti-tumor effect with no toxicity to normal cells. In this study, we evaluated the synergistic anti-tumor effect of oncolytic adenovirus ZD55-IL-24 combined with radiotherapy in prostate cancer. In Vitro and In Vivo experiments showed that the combined therapy significantly inhibited the growth of prostate cancer and provoked apoptosis of prostate cancer cells. In conclusion, the combination of ionizing radiation and oncolytic adenovirus expressing IL24 could achieve synergistic anti-tumor effect on prostate cancer, and is a promising strategy for prostate cancer therapy.

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CD31 regulates metastasis by inducing epithelial–mesenchymal transition in hepatocellular carcinoma via the ITGB1-FAK-Akt signaling pathway

Cited by 80 publications

References 51 publications

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

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

Long Non-coding RNA lnc-GNAT1-1 Suppresses Liver Cancer Progression via Modulation of Epithelial–Mesenchymal Transition

Combination Therapy of Prostate Cancer by Oncolytic Adenovirus Harboring Interleukin 24 and Ionizing Radiation

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