Homeobox D10, a tumor suppressor, inhibits the proliferation and migration of esophageal squamous cell carcinoma

Esophageal squamous cell carcinoma (ESCC) is one of the most common types of esophageal cancer, which is the sixth leading cause of cancer death globally. Homeobox D10 (HOXD10) is a member of the homeobox (HOX) gene family and has been reported to act as a tumor suppressor. However, the potential ro...

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Veröffentlicht in:Journal of cellular biochemistry 2019-08, Vol.120 (8), p.13717-13725
Hauptverfasser: Zhang, Jin, Liu, Shiyuan, Zhang, Danjie, Ma, Zhenchuan, Sun, Liangzhang
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container_issue 8
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container_title Journal of cellular biochemistry
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creator Zhang, Jin
Liu, Shiyuan
Zhang, Danjie
Ma, Zhenchuan
Sun, Liangzhang
description Esophageal squamous cell carcinoma (ESCC) is one of the most common types of esophageal cancer, which is the sixth leading cause of cancer death globally. Homeobox D10 (HOXD10) is a member of the homeobox (HOX) gene family and has been reported to act as a tumor suppressor. However, the potential role of HOXD10 in ESCC has not been reported. Thus, the aim of this study was to examine the expression and function of HOXD10 in ESCC. The expressions of HOXD10 in human ESCC tissues and cell lines were detected by quantitative reverse transcription polymerase chain reaction and Western blot. The HOXD10 overexpressing cell lines were established, then CCK‐8 and Transwell assays were performed to examine cell proliferation, migration, and invasion, respectively. The expression of EMT‐related proteins and signaling pathway‐related proteins were detected by Western blot. Our results showed that HOXD10 is lowly expressed in ESCC tissues as well as in ESCC cell lines. Ectopic overexpression of HOXD10 inhibited cell proliferation, migration, and invasion of ESCC cells (P 
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Homeobox D10 (HOXD10) is a member of the homeobox (HOX) gene family and has been reported to act as a tumor suppressor. However, the potential role of HOXD10 in ESCC has not been reported. Thus, the aim of this study was to examine the expression and function of HOXD10 in ESCC. The expressions of HOXD10 in human ESCC tissues and cell lines were detected by quantitative reverse transcription polymerase chain reaction and Western blot. The HOXD10 overexpressing cell lines were established, then CCK‐8 and Transwell assays were performed to examine cell proliferation, migration, and invasion, respectively. The expression of EMT‐related proteins and signaling pathway‐related proteins were detected by Western blot. Our results showed that HOXD10 is lowly expressed in ESCC tissues as well as in ESCC cell lines. Ectopic overexpression of HOXD10 inhibited cell proliferation, migration, and invasion of ESCC cells (P &lt; 0.05). HOXD10 overexpression repressed the epithelial‐mesenchymal transition (EMT) process in ESCC cells. Besides, HOXD10 overexpression suppressed the activation of PI3K/AKT/mTOR signaling pathway. PI3K/Akt agonist, insulin‐like growth factor‐1, reversed the inhibitory effects of HOXD10 on cell proliferation and migration in ESCC cells. Additional in vivo study proved that ectopic expression of HOXD10 caused an obvious inhibitory effect on the tumor growth. These findings indicated that overexpression of HOXD10 suppressed the proliferation, migration, and invasion via regulating the PI3K/AKT/mTOR signaling pathway in ESCC cells. Thus, targeting HOXD10 may be considered as a therapeutic strategy for ESCC treatment. Overexpression of HOXD10 suppressed the proliferation, migration, and invasion via regulating the PI3K/AKT/mTOR signaling pathway in ESCC cells. 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Homeobox D10 (HOXD10) is a member of the homeobox (HOX) gene family and has been reported to act as a tumor suppressor. However, the potential role of HOXD10 in ESCC has not been reported. Thus, the aim of this study was to examine the expression and function of HOXD10 in ESCC. The expressions of HOXD10 in human ESCC tissues and cell lines were detected by quantitative reverse transcription polymerase chain reaction and Western blot. The HOXD10 overexpressing cell lines were established, then CCK‐8 and Transwell assays were performed to examine cell proliferation, migration, and invasion, respectively. The expression of EMT‐related proteins and signaling pathway‐related proteins were detected by Western blot. Our results showed that HOXD10 is lowly expressed in ESCC tissues as well as in ESCC cell lines. Ectopic overexpression of HOXD10 inhibited cell proliferation, migration, and invasion of ESCC cells (P &lt; 0.05). HOXD10 overexpression repressed the epithelial‐mesenchymal transition (EMT) process in ESCC cells. Besides, HOXD10 overexpression suppressed the activation of PI3K/AKT/mTOR signaling pathway. PI3K/Akt agonist, insulin‐like growth factor‐1, reversed the inhibitory effects of HOXD10 on cell proliferation and migration in ESCC cells. Additional in vivo study proved that ectopic expression of HOXD10 caused an obvious inhibitory effect on the tumor growth. These findings indicated that overexpression of HOXD10 suppressed the proliferation, migration, and invasion via regulating the PI3K/AKT/mTOR signaling pathway in ESCC cells. Thus, targeting HOXD10 may be considered as a therapeutic strategy for ESCC treatment. Overexpression of HOXD10 suppressed the proliferation, migration, and invasion via regulating the PI3K/AKT/mTOR signaling pathway in ESCC cells. 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Homeobox D10 (HOXD10) is a member of the homeobox (HOX) gene family and has been reported to act as a tumor suppressor. However, the potential role of HOXD10 in ESCC has not been reported. Thus, the aim of this study was to examine the expression and function of HOXD10 in ESCC. The expressions of HOXD10 in human ESCC tissues and cell lines were detected by quantitative reverse transcription polymerase chain reaction and Western blot. The HOXD10 overexpressing cell lines were established, then CCK‐8 and Transwell assays were performed to examine cell proliferation, migration, and invasion, respectively. The expression of EMT‐related proteins and signaling pathway‐related proteins were detected by Western blot. Our results showed that HOXD10 is lowly expressed in ESCC tissues as well as in ESCC cell lines. Ectopic overexpression of HOXD10 inhibited cell proliferation, migration, and invasion of ESCC cells (P &lt; 0.05). HOXD10 overexpression repressed the epithelial‐mesenchymal transition (EMT) process in ESCC cells. Besides, HOXD10 overexpression suppressed the activation of PI3K/AKT/mTOR signaling pathway. PI3K/Akt agonist, insulin‐like growth factor‐1, reversed the inhibitory effects of HOXD10 on cell proliferation and migration in ESCC cells. Additional in vivo study proved that ectopic expression of HOXD10 caused an obvious inhibitory effect on the tumor growth. These findings indicated that overexpression of HOXD10 suppressed the proliferation, migration, and invasion via regulating the PI3K/AKT/mTOR signaling pathway in ESCC cells. Thus, targeting HOXD10 may be considered as a therapeutic strategy for ESCC treatment. Overexpression of HOXD10 suppressed the proliferation, migration, and invasion via regulating the PI3K/AKT/mTOR signaling pathway in ESCC cells. Thus, targeting HOXD10 may be considered as a therapeutic strategy for ESCC treatment.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>30938888</pmid><doi>10.1002/jcb.28644</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-0093-4121</orcidid></addata></record>
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subjects 1-Phosphatidylinositol 3-kinase
AKT protein
Biotechnology
Cancer
Cell growth
Cell migration
Cell proliferation
Cholecystokinin
Ectopic expression
epithelial‐mesenchymal transition (EMT)
Esophageal cancer
esophageal squamous cell carcinoma (ESCC)
Esophagus
Growth factors
Homeobox
Homeobox D10 (HOXD10)
In vivo methods and tests
Insulin
invasion
Kinases
Mesenchyme
migration
PI3K/AKT/mTOR signaling pathway
Polymerase chain reaction
Proteins
Reverse transcription
Signal transduction
Signaling
Squamous cell carcinoma
TOR protein
Tumor suppressor genes
Tumors
title Homeobox D10, a tumor suppressor, inhibits the proliferation and migration of esophageal squamous cell carcinoma
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