Overexpression of SULT2B1b Promotes Angiogenesis in Human Gastric Cancer

Chen, Wen; Zhou, Haiyu; Ye, Lei; Zhan, Baogen

doi:10.1159/000443055

Cited by 20 publications

(19 citation statements)

References 41 publications

(37 reference statements)

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“…It has been demonstrated that SULT2B1b activity increases gastric cancer angiogenesis and tumor volume, SULT2B1b activity promotes hepatocellular carcinoma cell growth in vitro and in vivo , and SULT2B1b expression correlates with poor prognosis and promotes tumor cell growth in colorectal cancer patients. (17,18,20) In fact, the Human Protein Atlas database (http://www.proteinatlas.org/ENSG00000088002-SULT2B1/cancer) of tissue samples supports elevated expression levels of SULT2B1b in PCa compared to normal tissue. As a result of the controversial role of SULT2B1b activity, additional studies in PCa are required to fully understand its function.…”

Section: Discussionmentioning

confidence: 99%

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Cholesterol Sulfonation Enzyme, SULT2B1b, Modulates AR and Cell Growth Properties in Prostate Cancer

Vickman

Crist

Kerian

et al. 2016

Molecular Cancer Research

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Cholesterol accumulates in prostate lesions and has been linked to prostate cancer (PCa) incidence and progression. However, how accumulated cholesterol contributes to PCa development and progression is not completely understood. Cholesterol sulfate (CS), the primary sulfonation product of cholesterol sulfotransferase (SULT2B1b), accumulates in human prostate adenocarcinoma and precancerous prostatic intraepithelial neoplasia (PIN) lesions compared to normal regions of the same tissue sample. Given the enhanced accumulation of CS in these lesions, it was hypothesized that SULT2B1b-mediated production of CS provides a growth advantage to these cells. To address this, PCa cells with RNAi-mediated knockdown (KD) of SULT2B1b were used to assess the impact on cell growth and survival. SULT2B1b is expressed and functional in a variety of prostate cells and the data demonstrate that SULT2B1b KD, in LNCaP and other androgen-responsive (VCaP and C4-2) cells, results in decreased cell growth/viability and induces cell death. SULT2B1b KD also decreases androgen receptor (AR) activity and expression at mRNA and protein levels. While AR overexpression has no impact on SULT2B1b KD-mediated cell death, addition of exogenous androgen is able to partially rescue the growth inhibition induced by SULT2B1b KD in LNCaP cells. These results suggest that SULT2B1b positively regulates the AR either through alterations in ligand availability or by interaction with critical co-regulators that influence AR activity. Implications These findings provide evidence that SULT2B1b is a novel regulator of AR activity and cell growth in prostate cancer and should be further investigated for therapeutic potential.

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Section: Discussionmentioning

confidence: 99%

“…Studies have shown a potential role of SULT2B1b in the growth and progression of cancer cells(17–20). SULT2B1b was studied in PCa in androgen-free conditions supplemented with DHEA(19,21).…”

Section: Introductionmentioning

confidence: 99%

Cholesterol Sulfonation Enzyme, SULT2B1b, Modulates AR and Cell Growth Properties in Prostate Cancer

Vickman

Crist

Kerian

et al. 2016

Molecular Cancer Research

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“…Hu et al [ 25 ] demonstrated that SULT2B1b expression is increased in colorectal carcinoma (CRC) and CRC-derived cell lines, and SULT2B1b overexpression promotes the growth and invasion of CRC cells. SULT2B1b is significantly overexpressed in gastric cancer (GC) and SULT2B1b overexpression promoted the angiogenesis and tumor growth in a GC mice model [ 26 ]. The UALCAN database indicates that SULT2B1 expression is also upregulated in cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

Verteporfin Promotes the Apoptosis and Inhibits the Proliferation, Migration, and Invasion of Cervical Cancer Cells by Downregulating SULT2B1 Expression

Yin

Chen

2020

Med Sci Monit

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Background Cervical cancer threatens women’s health worldwide. Verteporfin (VP), a small-molecule YAP1 inhibitor, inhibits cancer cell growth. This study investigated whether VP could inhibit the proliferation and promote the apoptosis of cervical cancer cells by decreasing SULT2B1 expression. Material/Methods Normal and cancerous cervical cell proliferation after VP treatment was detected by CCK-8 assay. HeLa cell migration, invasion, and apoptosis after VP treatment and transfection were analyzed by wound healing assay, transwell assay, and TUNEL assay, respectively. The expression of related proteins was determined by western blot analysis. Western blot and RT-qPCR analysis detected mRNA and protein expression of SULT2B1. Results Different VP concentrations (0.5, 1, 2, and 5 μM) inhibited the viability of HeLa cells and had no obvious effect on H8 cells. Therefore, 5 μM VP was selected for subsequent experiments. VP inhibited the proliferation, migration, and invasion of HeLa cells and promoted their apoptosis. Bcl-2 expression decreased, and expression of Bax, caspase-3, and caspase-9 in VP-treated HeLa cells increased. SULT2B1 expression increased in cervical cancer cells compared with normal cervical cells. Furthermore, SULT2B1 expression increased in HeLa cells and VP suppressed SULT2B1 expression. SULT2B1 overexpression reduced the inhibiting effect of VP on the proliferation, migration, and apoptosis of HeLa cells, and reduced VP effect on apoptosis of HeLa cells. SULT2B1 overexpression upregulated the Bcl-2 expression and downregulated the expression of Bax, caspase-3, and caspase-9 in VP-treated HeLa cells. Conclusions VP inhibited the proliferation, migration, and invasion and promoted apoptosis of cervical cancer cells by decreasing SULT2B1 expression.

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“…CS may also inhibit T cell function by displacing cholesterol from cell membrane and therefore compromising T cell receptor signaling . SULT2B1b may also alter the surrounding vasculature by modulating the production of angiogenic factors such as VEGF . Thus, the high level of SULT2B1b in the prostate epithelium may not only be beneficial for the epithelium but also be important for the stability of the tissue microenvironment.…”

Section: Discussionmentioning

confidence: 99%

Distinct expression patterns of SULT2B1b in human prostate epithelium

et al. 2019

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Background SULT2B1b (sulfotransferase family cytosolic 2B member 1b) catalyzes the sulfate conjugation of substrates such as cholesterol and oxysterols. Our laboratory has previously shown that SULT2B1b inhibition modulates androgen receptor signaling and induces apoptosis in prostate cancer cells. However, the functions of SULT2B1b in the prostate remain poorly understood. Methods We characterized the expression pattern of SULT2B1b in human benign prostate hyperplasia (BPH) as well as prostate cancer to determine the relationship between SULT2B1b and prostate diseases, using immunohistochemistry, immunofluorescence staining, immunoblot, and real‐time polymerase chain reaction. Results SULT2B1b was strongly detected in the prostate epithelium but was absent in the stroma. Significantly lower SULT2B1b was found in primary cancer cells compared with adjacent normal epithelial cells. SULT2B1b further decreased in metastatic cancer cells. Most interestingly, we found, for the first time, that SULT2B1b was much more concentrated in the luminal layer than in the basal layer in both normal prostate and BPH samples. The stronger presence of SULT2B1b in luminal epithelial cells was confirmed by costaining with luminal and basal markers and in sorted paired luminal and basal cells. SULT2B1b expression was induced with prostate organoid differentiation. Conclusions SULT2B1b inversely correlates with prostate cancer status, with the highest level in the normal epithelium and lowest in the advanced metastatic prostate cancer. Furthermore, SULT2B1b is mostly located within the luminal layer of the prostate epithelium, suggesting that it may be implicated in luminal differentiation.

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Overexpression of SULT2B1b Promotes Angiogenesis in Human Gastric Cancer

Cited by 20 publications

References 41 publications

Cholesterol Sulfonation Enzyme, SULT2B1b, Modulates AR and Cell Growth Properties in Prostate Cancer

Cholesterol Sulfonation Enzyme, SULT2B1b, Modulates AR and Cell Growth Properties in Prostate Cancer

Verteporfin Promotes the Apoptosis and Inhibits the Proliferation, Migration, and Invasion of Cervical Cancer Cells by Downregulating SULT2B1 Expression

Distinct expression patterns of SULT2B1b in human prostate epithelium

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