Corrigendum: Development and Validation of Novel Nomograms to Predict the Overall Survival and Cancer-Specific Survival of Cervical Cancer Patients With Lymph Node Metastasis

Yi, Jianying; Liu, Zhili; Wang, Lu; Zhang, Xingxin; Pi, Lili; Zhou, Chunlei; Mu, Hong

doi:10.3389/fonc.2022.916310

Cited by 2 publications

(1 citation statement)

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“…Tumor metastasis is the leading cause of cancer-related deaths globally, in which lymphangiogenesis and lymph node metastasis have been found to play a significant role [ 15 ]. However, the precise molecular and cellular regulators involved in lymphangiogenesis remain poorly understood.…”

Section: Discussionmentioning

confidence: 99%

The novel oncogenic factor TET3 combines with AHR to promote thyroid cancer lymphangiogenesis via the HIF-1α/VEGF signaling pathway

Yang,

Zhao,

Qiao

et al. 2023

Cancer Cell Int

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Background Lymphangiogenesis has been reported to play crucial roles in the metastasis of thyroid cancer (THCA), but despite the significant research on lymphangiogenesis in THCA, the precise regulatory mechanism remains unclear. Methods Public databases including the Cancer Genome Atlas (TCGA), TIMER, and UALCAN were used to analyze and visualize the expression of TET3 and AHR in THCA, and the correlation between these molecules were used by TIMER. Additionally, RT-PCR and Western Blot were performed to determine the mRNA and protein expression of related proteins. Plate colony formation, wound healing, cell cycle, apoptosis, angiogenesis and transwell assay were used to examine the ability of proliferation, movement, lymphangiogenesis, migration and invasion of THCA cells. Results Analysis of the TCGA database revealed higher expression levels of TET3 and AHR in tumor tissue compared to normal tissue in THCA. Additionally, a strong correlation was observed between TET3 and AHR. UALCAN database demonstrated that high expression of TET3 and AHR was associated with advanced THCA TNM stages in THCA patients. Furthermore, TET3 activation accelerated THCA cell proliferation by inducing G2/M phase arrest and suppressing apoptosis, while AHR inactivation reduced THCA cell proliferation by decreasing G2/M phase arrest and promoting apoptosis in vitro. Notably, both TET3 and AHR significantly enhanced THCA cell lymphangiogenesis, migration and invasion. Moreover, TET3 activation and AHR inactivation regulated HIF-1α/VEGF signaling pathway, which ultimately, blocked the HIF-1α/VEGF in THCA cells and impaired their movement, migration and invasion abilities. Conclusions The combined action of TET3 and AHR to promote lymphangiogenesis in THCA through the HIF-1α/VEGF signaling pathway, and targeting them might provide a potential treatment strategy for THCA.

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Section: Discussionmentioning

confidence: 99%

The novel oncogenic factor TET3 combines with AHR to promote thyroid cancer lymphangiogenesis via the HIF-1α/VEGF signaling pathway

Yang,

Zhao,

Qiao

et al. 2023

Cancer Cell Int

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The novel oncogenic factor TET3 combined AHR to promote Thyroid cancer lymphangiogenesis via HIF-1α/VEGF signaling pathway

Yang

Zhao

Qiao

et al. 2023

Preprint

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Background Lymphangiogenesis is an important factor in the invasion and metastasis of thyroid cancer (THCA). The relative researches of lymphangiogenesis have always been a hot topic in THCA, but its specific regulatory mechanism has not been totally clear. Methods Public databases including the Cancer Genome Atlas (TCGA), TIMER, GEPIA, and UALCAN database were employed to analyze and visualize the expression and prognosis of TET3 and AHR in THCA. GEPIA and TIMER were used to analyze the correlation between these molecules. Rt-PCR and Western Blot were used to detect the mRNA and protein expression of related proteins. Plate colony formation, cycle, apoptosis, angiogenesis and transwell assay were used to examine the ability of proliferation, lymphangiogenesis and invasion of THCA cells. Results TCGA database were showed that TET3 and AHR in tumor tissue compared to normal tissue in THCA. And there was a high correlation between TET3 and AHR. UALCAN and GEPIA database were exhibited that high expression of TET3 and AHR were corelated with THCA TNM stages and poor prognosis of THCA patients. Moreover, the TET3 activation accelerated THCA cells proliferation by inducing G2/M phase arrest and restraining apoptosis, and the AHR inactivation reduced THCA cells proliferation by decreasing G2/M phase arrest and inducing apoptosis in vitro of THCA cells. Notably, TET3 and AHR markedly promoted THCA cells lymphangiogenesis and invasion. In addition, TET3 activation and AHR inactivation regulated HIF-1α/VEGF signaling pathway. Conclusions TET3 combined AHR to promote THCA lymphangiogenesis via HIF-1α/VEGF signaling pathway and targeting TET3 and AHR might provide a potential treatment strategy for THCA.

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Corrigendum: Development and Validation of Novel Nomograms to Predict the Overall Survival and Cancer-Specific Survival of Cervical Cancer Patients With Lymph Node Metastasis

Cited by 2 publications

References 0 publications

The novel oncogenic factor TET3 combines with AHR to promote thyroid cancer lymphangiogenesis via the HIF-1α/VEGF signaling pathway

The novel oncogenic factor TET3 combines with AHR to promote thyroid cancer lymphangiogenesis via the HIF-1α/VEGF signaling pathway

The novel oncogenic factor TET3 combined AHR to promote Thyroid cancer lymphangiogenesis via HIF-1α/VEGF signaling pathway

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