SLC35B2 Expression is Associated with a Poor Prognosis of Invasive Ductal Breast Carcinoma

Chim-ong, Anongruk; Thawornkuno, Charin; Chavalitshewinkoon-Petmitr, Porntip; Punyarit, Phaibul; Petmitr, Songsak

doi:10.7314/apjcp.2014.15.15.6065

Cited by 3 publications

(2 citation statements)

References 37 publications

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“…Besides PDAC, increased SLC35B2 expression has been reported to correlate with poor prognosis of invasive ductal breast carcinoma, 39 whereas knockdown of SLC35B2 decreases the proliferation of the human colon cancer DLD-1 cells in vitro. 40 It is interesting to know whether ITGB4 also is sulfonated in other cancer types, and, if so, whether the sulfation of ITGB4 contributes to the growth-inhibitory effect of SLC35B2 knockdown in non-PDAC cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of the SLC35B2–TPST2 Axis of Tyrosine Sulfation Attenuates the Growth and Metastasis of Pancreatic Ductal Adenocarcinom

Cai¹,

Li²,

Zeng³

et al. 2023

Cellular and Molecular Gastroenterology and Hepatology

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Section: Discussionmentioning

confidence: 99%

Inhibition of the SLC35B2–TPST2 Axis of Tyrosine Sulfation Attenuates the Growth and Metastasis of Pancreatic Ductal Adenocarcinom

Cai¹,

Li²,

Zeng³

et al. 2023

Cellular and Molecular Gastroenterology and Hepatology

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“…Cartilage defects and lethal phenotypes have been linked to Slc35b2 in Zebrafish and Drosophila (Kamiyama et al, 2003;Clément et al, 2008), whereas up-regulation of SLC35B2 mRNA expression is associated with poor prognosis of invasive ductal breast carcinoma in humans (Chim-ong et al, 2014).…”

Section: Paps Synthetase and Transporter Genesmentioning

confidence: 99%

Genetics and pathophysiology of mammalian sulfate biology

Langford

Hurrion

Dawson

2017

Journal of Genetics and Genomics

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Nutrient sulfate is essential for numerous physiological functions in mammalian growth and development. Accordingly, disruptions to any of the molecular processes that maintain the required biological ratio of sulfonated and unconjugated substrates are likely to have detrimental consequences for mammalian physiology. Molecular processes of sulfate biology can be broadly grouped into four categories: firstly, intracellular sulfate levels are maintained by intermediary metabolism and sulfate transporters that mediate the transfer of sulfate across the plasma membrane; secondly, sulfate is converted to 3'-phosphoadenosine 5'-phosphosulfate (PAPS), which is the universal sulfonate donor for all sulfonation reactions; thirdly, sulfotransferases mediate the intracellular sulfonation of endogenous and exogenous substrates; fourthly, sulfate is removed from substrates via sulfatases. From the literature, we curated 91 human genes that encode all known sulfate transporters, enzymes in pathways of sulfate generation, PAPS synthetases and transporters, sulfotransferases and sulfatases, with a focus on genes that are linked to human and animal pathophysiology. The predominant clinical features linked to these genes include neurological dysfunction, skeletal dysplasias, reduced fecundity and reproduction, and cardiovascular pathologies. Collectively, this review provides reference information for genetic investigations of perturbed mammalian sulfate biology.

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Solute Carrier Family 35 (SLC35)—An Overview and Recent Progress

Kamiyama,

Sone

2024

Biologics

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The solute carrier family 35 (SLC35) comprises multiple members of transporters, including a group of proteins known as nucleotide sugar transporters (NSTs), an adenosine triphosphate (ATP) transporter, 3′-phosphoadenosine 5′-phosphosulfate (PAPS) transporters, and transporters of unknown function. To date, seven subfamilies (A to G) and 32 members have been classified into this large SLC35 family. Since the majority of glycosylation reactions occur within the lumen of the endoplasmic reticulum (ER) and Golgi apparatus, the functions of NSTs are indispensable for the delivery of substrates for glycosylation. Recent studies have revealed the diverse functions of this family of proteins in the regulation of numerous biological processes, including development, differentiation, proliferation, and disease progression. Furthermore, several congenital disorders of glycosylation (CDGs) resulting from variations in the SLC35 family member genes have been identified. To elucidate the pathology of these diseases, a variety of knockout mice harboring mutations in the family member genes have been generated and employed as animal models for CDGs. This review presents a historical overview of the SLC35 family, with a particular focus on recent advances in research on the functions of this family and their relationship to human diseases.

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SLC35B2 Expression is Associated with a Poor Prognosis of Invasive Ductal Breast Carcinoma

Cited by 3 publications

References 37 publications

Inhibition of the SLC35B2–TPST2 Axis of Tyrosine Sulfation Attenuates the Growth and Metastasis of Pancreatic Ductal Adenocarcinom

Inhibition of the SLC35B2–TPST2 Axis of Tyrosine Sulfation Attenuates the Growth and Metastasis of Pancreatic Ductal Adenocarcinom

Genetics and pathophysiology of mammalian sulfate biology

Solute Carrier Family 35 (SLC35)—An Overview and Recent Progress

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