Increased expression of<i>Solute carrier family 12 member 5</i>via gene amplification contributes to tumour progression and metastasis and associates with poor survival in colorectal cancer

Xu, Lixia; Li, Xiaoxing; Cai, Mengli; Chen, Jinna; Li, Xiangchun; Wu, William Ka Kei; Kang, Wei; Tong, Joanna H.M.; To, Ka Fai; Guan, Xin Yuan; Sung, Joseph J.Y.; Chan, Francis K.L.; Yu, Jun

doi:10.1136/gutjnl-2014-308257

Cited by 44 publications

(45 citation statements)

References 47 publications

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“…In clinical practice, many oncologists have realized that the TNM staging system alone does not have the optimal predictive value in several human cancers, including ESCC [7,38,39], consistent with our findings. Consequently, additional prognostic biomarkers are required to improve the risk assessment of the TNM staging system.…”

Section: Discussionsupporting

confidence: 82%

Predictive Value of LINC01133 for Unfavorable Prognosis was Impacted by Alcohol in Esophageal Squamous Cell Carcinoma

Yang

Tien

et al. 2018

Cell Physiol Biochem

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Background/Aims: Considerable evidence indicates that long noncoding RNAs (lncRNAs) exert importantly regulatory functions during human cancer initiation and progression and are promising biotargets in the flight against cancer. Methods: In this study, we evaluated the role of the lncRNA LINC01133 in esophageal squamous cell carcinoma (ESCC). LINC01133 expression in ESCC was examined by quantitative real-time PCR. The correlations between LINC01133 expression and clinicopathological variables and survival were examined by the χ² test, Kaplan–Meier method, log-rank test, and univariate Cox regression analysis. Results: LINC01133 expression levels were frequently lower in ESCC tissues and cell lines than in paired normal tissues and an immortalized esophageal epithelial cell line, respectively. The expression of LINC01133 decreased in a TNM stage- and lifestyle-independent manner. LINC01133 was an independent protective factor and had an anti-tumor effect in the early stage of ESCC development. More importantly, we discovered that drinking status in our cohort impaired the predictive accuracy of LINC01133 for patients with ESCC. Furthermore, a new risk model combining LINC01133 expression, drinking status, and TNM stage provided better survival discrimination compared with three other predictors. Conclusions: Our data indicate that a loss of LINC01133 expression is a potential poor prognostic biomarker and therapeutic target for ESCC and provide additional prognostic information to improve the outcomes of ESCC patients.

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Section: Discussionsupporting

confidence: 82%

Predictive Value of LINC01133 for Unfavorable Prognosis was Impacted by Alcohol in Esophageal Squamous Cell Carcinoma

Yang

Tien

et al. 2018

Cell Physiol Biochem

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“…Chromosome 20q amplification has been commonly found in colorectal cancer and is involved in transforming adenoma to carcinoma (5,6). Chromosome 20q amplification is also a potential indicator of poor prognosis in patients with colorectal cancer (7)(8)(9). By whole-genome sequencing (WGS), we identified that TTPAL (tocopherol alpha transfer protein-like), located at 20q13.12, was preferentially amplified in primary colorectal tumor tissues.…”

Section: Introductionmentioning

confidence: 97%

TTPAL Promotes Colorectal Tumorigenesis by Stabilizing TRIP6 to Activate Wnt/β-Catenin Signaling

et al. 2019

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Copy number alterations are crucial for the development of colorectal cancer. Our whole-genome analysis identified tocopherol alpha transfer protein-like (TTPAL) as preferentially amplified in colorectal cancer. Here we demonstrate that frequent copy number gain of TTPAL leads to gene overexpression in colorectal cancer from a Chinese cohort (n ¼ 102), which was further validated by a The Cancer Genome Atlas (TCGA) cohort (n ¼ 376). High expression of TTPAL was significantly associated with shortened survival in patients with colorectal cancer. TTPAL promoted cell viability and clonogenicity, accelerated cell-cycle progression, inhibited cell apoptosis, increased cell migration/invasion ability in vitro, and promoted tumorigenicity and cancer metastasis in vivo. TTPAL significantly activated Wnt signaling and increased b-catenin activation and protein expression of cyclin D1 and c-Myc. Coimmunoprecipitation followed by mass spectrometry identified thyroid receptorinteracting protein 6 (TRIP6) as a direct downstream effector of TTPAL. Depletion of TRIP6 significantly abolished the effects of TTPAL on cell proliferation and Wnt activation. Direct binding of TTPAL with TRIP6 in the cytoplasm inhibited ubiquitinmediated degradation of TRIP6 and, subsequently, increased levels of TRIP6 displaced b-catenin from the tumor suppressor MAGI1 via competitive binding. This sequence of events allows b-catenin to enter the nucleus and promotes oncogenic Wnt/ b-catenin signaling. In conclusion, TTPAL is commonly overexpressed in colorectal cancer due to copy number gain, which promotes colorectal tumorigenesis by activating Wnt/b-catenin signaling via stabilization of TRIP6. TTPAL overexpression may serve as an independent new biomarker for the prognosis of patients with colorectal cancer.Significance: TTPAL, a gene preferentially amplified in colorectal cancer, promotes colon tumorigenesis via activation of the Wnt/b-catenin pathway.

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“…The SLC gene superfamily controls essential physiological functions and its disturbance may result in diseases like malignancies. For example, Xu et al found that amplification of SLC12A5 plays a strong tumorigenic role and is associated with poor prognosis of patients with colorectal cancer . SLC39A6 promotes aggressiveness of esophageal squamous carcinoma cells by increasing intracellular levels of zinc and activates phosphatidylinositol 3‐kinase (PI3K) pathway .…”

Section: Introductionmentioning

confidence: 99%

“…For example, Xu et al found that amplification of SLC12A5 plays a strong tumorigenic role and is associated with poor prognosis of patients with colorectal cancer. 6 SLC39A6 promotes aggressiveness of esophageal squamous carcinoma cells by increasing intracellular levels of zinc and activates phosphatidylinositol 3-kinase (PI3K) pathway. 7 SLC35, a group of nucleotide sugar transporters, currently comprises at least 31 homologous molecular species from SLC35A to SLC35G.…”

Section: Introductionmentioning

confidence: 99%

Solute carrier family 35 member F2 is indispensable for papillary thyroid carcinoma progression through activation of transforming growth factor‐β type I receptor/apoptosis signal‐regulating kinase 1/mitogen‐activated protein kinase signaling axis

Jin

Zhou

et al. 2018

Cancer Science

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Solute carrier family members control essential physiological functions and are tightly linked to human diseases. Solute carrier family 35 member F2 (SLC35F2) is aberrantly activated in several malignancies. However, the biological function and molecular mechanism of SLC35F2 in papillary thyroid carcinoma (PTC) are yet to be fully explored. Here, we showed that SLC35F2 was prominently upregulated in PTC tissues at both protein and mRNA expression level compared with matched adjacent normal tissues. Besides, the high expression of SLC35F2 was significantly associated with lymph node metastasis in patients with PTC. CRISPR/Cas9‐mediated knockout of SLC35F2 attenuated the tumorigenic properties of PTC, including cell proliferation, migration and invasion and induced G1 phase arrest. In contrast, ectopic expression of SLC35F2 brought about aggressive malignant phenotypes of PTC cells. Moreover, SLC35F2 expedited the proliferation and migration of PTC cells by targeting transforming growth factor‐β type I receptor (TGFBR1) and phosphorylation of apoptosis signal‐regulating kinase 1 (p‐ASK‐1), thereby activating the mitogen‐activated protein kinase signaling pathway. The malignant behaviors induced by overexpression of SLC35F2 could be abrogated by silencing of TGFBR1 using a specific inhibitor. We conducted the first study on SLC35F2 in thyroid cancer with the aim of elucidating the functional significance and molecular mechanism of SLC35F2. Our findings suggest that SLC35F2 exerts its oncogenic effect on PTC progression through the mitogen‐activated protein kinase pathway, with dependence on activation of TGFBR‐1 and apoptosis signal‐regulating kinase 1.

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Increased expression ofSolute carrier family 12 member 5via gene amplification contributes to tumour progression and metastasis and associates with poor survival in colorectal cancer

Cited by 44 publications

References 47 publications

Predictive Value of LINC01133 for Unfavorable Prognosis was Impacted by Alcohol in Esophageal Squamous Cell Carcinoma

Predictive Value of LINC01133 for Unfavorable Prognosis was Impacted by Alcohol in Esophageal Squamous Cell Carcinoma

TTPAL Promotes Colorectal Tumorigenesis by Stabilizing TRIP6 to Activate Wnt/β-Catenin Signaling

Solute carrier family 35 member F2 is indispensable for papillary thyroid carcinoma progression through activation of transforming growth factor‐β type I receptor/apoptosis signal‐regulating kinase 1/mitogen‐activated protein kinase signaling axis

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