WNT5A promotes the metastasis of esophageal squamous cell carcinoma by activating the HDAC7/SNAIL signaling pathway

Feng, Yingtong; Ma, Zhiqiang; Pan, Minghong; Xu, Liqun; Feng, Junjun; Zhang, Yimeng; Shao, Changjian; Guo, Kai; Duan, Hongtao; Zhang, Yujing; Zhang, Yuxi; Zhang, Jiao; Lu, Da-Yong; Ren, Xiaoya; Han, Jing; Li, Xiaofei; Yan, Xiaolong

doi:10.1038/s41419-022-04901-x

Cited by 14 publications

(8 citation statements)

References 52 publications

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“…Studies have also reported that HDAC7 is crucial in cancer metastasis, for instance, in breast cancer, nasopharyngeal cancer, and ovarian cancer [17,22]. A previous study verified that HDAC7 dramatically increases Snail levels and decreases E-cadherin levels, further promoting the migration and invasion of ESCC [19]. Our current study revealed that HDAC7 overexpression promotes the metastasis of CM cells, which was validated by wound healing and transwell assays.…”

Section: Discussionsupporting

confidence: 81%

“…Dysregulated HDAC7 expression has been validated in various cancers, such as ovarian cancer, and glioma. HDAC7 overexpression contributes to migration and is linked with a poor prognosis in lung cancer, nasopharyngeal carcinoma, and esophageal squamous cell carcinoma (ESCC) [ 17 – 19 ]. In the present study, the IHC analysis results based on 16 paired CM tumors and normal samples showed that the HDAC7 level was significantly higher in CM tumor tissues.…”

Section: Discussionmentioning

confidence: 99%

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HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells

et al. 2023

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Choroidal melanoma (CM) is the most common type of diagnosed uveal melanoma (UM), which is prone to metastasis and exhibits a poor prognosis. The molecular mechanisms underlying CM progression need further elucidation to research effective therapeutic strategies. Histone deacetylase 7 (HDAC7) is very important in regulating cancer progression, but the significance and effect of HDAC7 on CM progression are unclear. In the present study, we found that HDAC7 is overexpressed in CM tissues versus normal tissues. We built HDAC7 overexpressing CM cell lines to study the functions of HDAC7 in CM progression and verified that upregulation of HDAC7 promoted the proliferation and metastasis of CM cells, while pharmacological inhibition of HDAC7 suppressed both the proliferation and metastasis of CM cells. Furthermore, we found that the aforementioned cancer-promoting effect of HDAC7 was mediated by c-Myc. Targeted inhibition of c-Myc inhibited CM progression by interfering with the HDAC7/c-Myc signaling pathway. Our study highlighted the function of targeting the HDAC7/c-Myc signaling pathway to intervene in the pathological process of CM, which provides potential therapeutic strategies for CM treatment.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells

et al. 2023

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“…Regarding the mechanisms through which EMT is induced by HDAC7 or TTYH3, further investigations have yet been conducted by us. However, Feng et al 34 demonstrated the impact of HDAC7 on EMT by upregulating Snail. Specially, Wang et al 14 have reported that TTYH3 can impact EMT through GSK3-β/β-catenin pathway in hepatocellular carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Tweety homolog 3 promotes colorectal cancer progression through mutual regulation of histone deacetylase 7

Lu,

Deng,

Liu

et al. 2024

MedComm

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Colorectal cancer (CRC) is one of the leading cancers worldwide, with metastasis being a major cause of high mortality rates among patients. In this study, dysregulated gene Tweety homolog 3 (TTYH3) was identified by Gene Expression Omnibus database. Public databases were used to predict potential competing endogenous RNAs (ceRNAs) for TTYH3. Quantitative real‐time polymerase chain reaction, western blot, and immunohistochemistry were utilized to analyze TTYH3 and histone deacetylase 7 (HDAC7) levels. Luciferase assays confirmed miR‐1271‐5p directly targeting the 3′ untranslated regions of TTYH3 and HDAC7. In vitro experiments such as transwell and human umbilical vein endothelial cell tube formation, as well as in vivo mouse models, were conducted to assess the biological functions of TTYH3 and HDAC7. We discovered that upregulation of TTYH3 in CRC promotes cell migration by affecting the Epithelial–mesenchymal transition pathway, which was independent of its ion channel activity. Mechanistically, TTYH3 and HDAC7 functioned as ceRNAs, reciprocally regulating each other's expression. TTYH3 competes for binding miR‐1271‐5p, increasing HDAC7 expression, facilitating CRC metastasis and angiogenesis. This study reveals the critical role of TTYH3 in promoting CRC metastasis through ceRNA crosstalk, offering new insights into potential therapeutic targets for clinical intervention.

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“…This study also demonstrated that melatonin, a hormone produced by the pineal gland, could hinder the growth of ESCC tumor by reducing the activity of the HDAC7/β-catenin/c-myc positive feedback loop and suppressing the function of USP10 that is responsible for maintaining the stability of HDAC7 protein ( 35 ). An additional mechanism of ESCC has been elucidated, indicating the involvement of HDAC7 in the metastasis of tumor cells mediated by WNT5A ( 49 ). These studies reveal tumorigenesis originates from the loss of the body’s constraints on oncogenic factors.…”

Section: The Involvement Of Hdac7 In Cancermentioning

confidence: 99%

HDAC7: a promising target in cancer

Liu,

Zheng,

et al. 2024

Front. Oncol.

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Histones have a vital function as components of nucleosomes, which serve as the fundamental building blocks of chromatin. Histone deacetylases (HDACs), which target histones, suppress gene transcription by compacting chromatin. This implies that HDACs have a strong connection to the suppression of gene transcription. Histone deacetylase 7 (HDAC7), a member of the histone deacetylase family, may participate in multiple cellular pathophysiological processes and activate relevant signaling pathways to facilitate the progression of different tumors by exerting deacetylation. In recent years, HDAC7 has been increasingly studied in the pathogenesis of tumors. Studies that are pertinent have indicated that it has a significant impact on the growth and metastasis of tumors, the formation of the vascular microenvironment, and the emergence of resistance to drugs. Therefore, HDAC7 could potentially function as a potent predictor for tumor prognosis and a promising target for mitigating drug resistance in tumors. This review primarily concentrates on elucidating the structure and function of HDAC7, its involvement in the development of various tumors, and its interplay with relevant signaling pathways. Meanwhile, we briefly discuss the research direction and prospect of HDAC7.

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WNT5A promotes the metastasis of esophageal squamous cell carcinoma by activating the HDAC7/SNAIL signaling pathway

Cited by 14 publications

References 52 publications

HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells

HDAC7/c-Myc signaling pathway promotes the proliferation and metastasis of choroidal melanoma cells

Tweety homolog 3 promotes colorectal cancer progression through mutual regulation of histone deacetylase 7

HDAC7: a promising target in cancer

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