Long Noncoding RNA VESTAR Regulates Lymphangiogenesis and Lymph Node Metastasis of Esophageal Squamous Cell Carcinoma by Enhancing VEGFC mRNA Stability

Wang, Yali; Zhang, Weiyang; Liu, Wenzhong; Huang, Lijie; Wang, Yan; Li, Dan; Wang, Guangchao; Zhao, Zitong; Chi, Xinming; Yu, Xue; Song, Yongmei; Li, Xuefeng; Zhan, Qimin

doi:10.1158/0008-5472.can-20-1713

Cited by 40 publications

(31 citation statements)

References 54 publications

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“…As HuR is crucial for mRNA stability [ 27 ] and plays an oncogenic role in cancers [ 28 , 29 ], and GLUD1 mRNA and protein levels were down-regulated by HuR knockdown in this study (Fig. 5G, H ), we further explored the stability of GLUD1 mRNA by HuR knockdown followed by ACTD treatment, and found that the stability of GLUD1 mRNA was decreased in the SiHa and CaSki cells with HuR knockdown, compared with control cells (Fig.…”

Section: Resultsmentioning

confidence: 84%

Oncogenic circTICRR suppresses autophagy via binding to HuR protein and stabilizing GLUD1 mRNA in cervical cancer

et al. 2022

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Circular RNAs (circRNAs) are critical regulators in the occurrence and development of numerous cancers, in which abnormal autophagy plays a key role. However, the potential involvement of circRNAs in autophagy is largely unknown. Here, we identified the overexpression of circTICRR, a circular RNA, in cervical cancer. In vitro experiments showed that knockdown of circTICRR activated autophagy, and consequently promoted apoptosis and inhibited proliferation in cervical cancer cells, and vice versa. CircTICRR interacted with HuR protein via binding to F287/F289 in the RRM3 domain of HuR, stabilizing GLUD1 mRNA and elevating the level of GLUD1 protein. In vivo experiments revealed that knockdown of circTICRR suppressed the growth of transplanted tumors. An inhibitory peptide specific to the binding site between circTICRR and HuR protein promoted autophagy, induced apoptosis, suppressed proliferation in cervical cancer cells, and inhibited the growth of xenografts. Our findings suggest that circTICRR acts as an oncogene in cervical cancer and the interaction between circTICRR and HuR protein may be a potential target in cervical cancer therapeutics.

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Section: Resultsmentioning

confidence: 84%

Oncogenic circTICRR suppresses autophagy via binding to HuR protein and stabilizing GLUD1 mRNA in cervical cancer

et al. 2022

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“…VESTAR interacts with HuR to promote the binding of HuR to VEGF-C mRNA. Therefore, VESTAR -mediated VEGF-C mRNA stability may be an important contributor to lymph node metastasis in ESCC and could be a novel target for the diagnosis and treatment of tumor metastasis ( 42 ).…”

Section: Long-chain Non-coding Rnas Promote the Occurrence And Develo...mentioning

confidence: 99%

Long Non-Coding RNA in Esophageal Cancer: A Review of Research Progress

Yang¹,

Chen²

2022

Pathol. Oncol. Res.

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In recent years, there has been significant progress in the diagnosis and treatment of esophageal cancer. However, owing to the lack of early diagnosis strategies and treatment targets, the prognosis of patients with esophageal cancer remains unsatisfactory. There is an urgent need to identify novel biomarkers and treatment targets for esophageal cancer. With the development of genomics, long-chain non-coding RNAs (LncRNAs), which were once considered transcriptional “noise,” are being identified and characterized rapidly in large numbers. Recent research shows that LncRNAs are closely related to a series of steps in tumor development and play an important regulatory role in DNA replication, transcription, and post-transcriptional regulation. The abnormal expression of LncRNAs leads to tumor cell proliferation, migration, invasion, and treatment resistance. This review focuses on the latest progress in research on the abnormal expression and functional mechanisms of LncRNAs in esophageal cancer. Further, it discusses the potential applications of these findings towards achieving an early diagnosis, improving treatment efficacy, and evaluating the prognosis of esophageal cancer.

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“…Esophageal carcinoma (EC) is one of the most malignant tumors worldwide, and present a great threat to the health of society [ 1 , 2 ]. EC is well known by its high rate of metastasis, aggressive invasion and poor prognosis [ 3 ]. Surgery and chemotherapy are effective treatments for EC diagnosed at an early stage, while a lot of EC patients comes to recurrence or metastasis, and eventually develop to advanced stages of cancers, which present poor prognosis [ 4 ].…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside compound K inhibits the proliferation, migration and invasion of Eca109 cell via VEGF-A/Pi3k/Akt pathway

Huang

Pan

Liu

et al. 2022

J Cardiothorac Surg

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Objective Esophageal cancer, one of the most common cancers in the upper digestive tract and is one of the leading cancer-related mortality worldwide. Accumulating studies found that Ginsenoside compound K (CK) has significantly anti-tumor effects, especially in the suppression of proliferation, migration, as well as invasion in various human cancers. While the effects of Ginsenoside CK in esophageal cancer have not been well studied. In our present study, we aim to explore the functions and mechanisms of Ginsenoside CK in the progression of esophageal cancer cells (Eca109). Methods Cell Counting Kit-8 (CCK-8), wound healing, transwell and flow cytometry assays were applied to analyze the effects of Ginsenoside CK in the progression of Eca109 cell, western blot assay was used to investigate the potential downstream signaling pathway after Ginsenoside CK treatment. Results Our study found that Ginsenoside CK can suppress cell proliferation, migration and invasion of Eca109 cell. Furthermore, the flow cytometry showed that Ginsenoside CK increased of apoptosis rates in Eca109 cell. The western blot results indicated that Ginsenoside CK decreased the expression of VEGF-A, P-Pi3k and P-Akt proteins. Moreover, the knockdown of VEGF-A gene could suppress cell proliferation, migration, invasion and induce apoptosis in Eca109 cell, and the expression of P-Pi3k and P-Akt proteins were significantly downregulated. Conclusions Our study suggests that Ginsenoside CK inhibits the proliferation, migration, invasion, and induced apoptosis of Eca109 cell by blocking VEGF-A/Pi3k/Akt signaling pathway.

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Long Noncoding RNA VESTAR Regulates Lymphangiogenesis and Lymph Node Metastasis of Esophageal Squamous Cell Carcinoma by Enhancing VEGFC mRNA Stability

Cited by 40 publications

References 54 publications

Oncogenic circTICRR suppresses autophagy via binding to HuR protein and stabilizing GLUD1 mRNA in cervical cancer

Oncogenic circTICRR suppresses autophagy via binding to HuR protein and stabilizing GLUD1 mRNA in cervical cancer

Long Non-Coding RNA in Esophageal Cancer: A Review of Research Progress

Ginsenoside compound K inhibits the proliferation, migration and invasion of Eca109 cell via VEGF-A/Pi3k/Akt pathway

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