The sialyltransferase ST3Gal3 facilitates the receptivity of the uterine endometrium <i>in vitro</i> and <i>in vivo</i>

Yu, Miao; Wang, Hao; Liu, Jianwei; Qin, Huamin; Liu, Shuai; Qiu, Yan

doi:10.1002/1873-3468.13252

Cited by 16 publications

(18 citation statements)

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“…Sialyltransferase is a biosynthetic enzyme of the sialic acid metabolic pathway mediating the transfer of sialic acid residues to various oligosaccharide chains found on glycoproteins and glycolipids. 32 The proper function of sialyltransferase leads to the formation of sialome. 6 Indeed, sialic acids are vital players in the modulation of cell functions and communications.…”

Section: Discussionmentioning

confidence: 99%

“…31 Furthermore, it has been reported that enhanced sLeX is associated with a better pregnancy outcome. 32 SLeX on the uterine epithelium has a role in implantation. 32 By carrying out segregation analysis in the family, we found that the mothers (IV.2 and IV.4) were heterozygote for the novel variant.…”

Section: Discussionmentioning

confidence: 99%

“…32 SLeX on the uterine epithelium has a role in implantation. 32 By carrying out segregation analysis in the family, we found that the mothers (IV.2 and IV.4) were heterozygote for the novel variant. Interestingly, the medical documents revealed that they had experienced several unsuccessful pregnancies (more than times).…”

Section: Discussionmentioning

confidence: 99%

“…There is some evidence indicating that ST3Gal3 plays a role in maintaining higher cognitive functions, regulating brain development and being involved in the inflammation process 31 . Furthermore, it has been reported that enhanced sLeX is associated with a better pregnancy outcome 32 . SLeX on the uterine epithelium has a role in implantation 32 .…”

Section: Discussionmentioning

confidence: 99%

“…groups, including mild (IQ of 55-70), moderate (IQ of 40-55), severe (IQ of[25][26][27][28][29][30][31][32][33][34][35][36][37][38][39][40] and profound (IQ of less than 25). Additionally, ID is divided into two major groups, including syndromic-and non-syndromic-ID.…”

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confidence: 99%

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A novel variant of ST3GAL3 causes non‐syndromic autosomal recessive intellectual disability in Iranian patients

Farajollahi

Razmara

Heidari

et al. 2020

The Journal of Gene Medicine

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Background: The number of reported genes causing non-syndromic autosomal recessive intellectual disability (NS-ARID) is increasing. For example, mutations in the ST3GAL3 gene have been reported to be associated with NS-ARID. In the present study, we aimed to determine the genetic cause of the NS-ARID in a five-generation consanguineous Iranian family. Methods: We subjected four patients with an initial diagnosis of NS-ID in an Iranian family. To identify the possible genetic cause(s), whole-exome sequencing was performed on the proband and Sanger sequencing was applied to investigate cosegregation analysis. Using in silico predictive tools, the possible impacts of the variant on the structure and function of ST3Gal-III were predicted. Results: The common clinical features were detected in all affected members who were suffering from a severe ID. Using whole-exome sequencing, a novel variant, c.704C>T or p.(Thr235Met), in exon 9 of the ST3GAL3 gene (NM_001270461.2, OMIM# 606494) was identified and verified by Sanger sequencing. This variant is located next to the VS motif of ST3Gal-III, which is a vital part of the catalytical domains. Conclusions: In the present study, we identified a novel missense variant, c.704C>T or p.(Thr235Met), in the ST3GAL3. To our knowledge, is the third variant in this gene to be associated with NS-ARID. Our findings highlight the need for further investigations into the mechanisms by which variants in ST3GAL3 contribute to neurological dysfunction.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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A novel variant of ST3GAL3 causes non‐syndromic autosomal recessive intellectual disability in Iranian patients

Farajollahi

Razmara

Heidari

et al. 2020

The Journal of Gene Medicine

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N‐glycosylation of uterine endometrium determines its receptivity

Qin

Wang

et al. 2019

Journal Cellular Physiology

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Glycosylation alters the molecular and functional features of glycoproteins, which is closely related with many physiological processes and diseases. During "window of implantation", uterine endometrium transforms into a receptive status to accept the embryo, thereby establishing successful embryo implantation. In this article, we aimed at investigating the role of N-glycosylation, a major modification type of glycoproteins, in the process of endometrial receptivity establishment. Results found that human uterine endometrial tissues at mid-secretory phase exhibited Lectin PHA-E+L (recognizes the branched N-glycans) positive N-glycans as measured by the Lectin fluorescent staining analysis. By utilizing in vitro implantation model, we found that de-N-glycosylation of human endometrial Ishikawa and RL95-2 cells by tunicamycin (inhibitor of N-glycosylation) and peptide-N-glycosidase F (PNGase F) impaired their receptive ability to human trophoblastic JAR cells. Meanwhile, N-glycosylation of integrin αvβ3 and leukemia inhibitory factor receptor (LIFR) are found to play key roles in regulating the ECM-dependent FAK/Paxillin and LIF-induced STAT3 signaling pathways, respectively, thus affecting the receptive potentials of endometrial cells. Furthermore, in vivo experiments and primary mouse endometrial cells-embryos coculture model further verified that N-glycosylation of mouse endometrial cells contributed to the successful implantation. Our results provide new evidence to show that N-glycosylation of uterine endometrium is essential for maintaining the receptive functions, which gives a better understanding of the glycobiology of implantation. K E Y W O R D S embryo implantation, endometrial receptivity, N-glycosylation, LIFR, avβ3

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ST3GalIV drives SLeX biosynthesis in gastrointestinal cancer cells and associates with cancer cell motility

et al. 2023

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Expression of sialyl Lewis X (SLeX) is a well-documented event during malignant transformation of cancer cells, and largely associates with their invasive and metastatic properties. Glycoproteins and glycolipids are the main carriers of SLeX, whose biosynthesis is known to be performed by different glycosyltransferases, namely by the family of β-galactoside-α2,3-sialyltransferases (ST3Gals). In this study, we sought to elucidate the role of ST3GalIV in the biosynthesis of SLeX and in malignant properties of gastrointestinal (GI) cancer cells. By immunofluorescent screening, we selected SLeX-positive GI cancer cell lines and silenced ST3GalIV expression via CRISPR/Cas9. Flow cytometry, immunofluorescence and western blot analysis showed that ST3GalIV KO efficiently impaired SLeX expression in most cancer cell lines, with the exception of the colon cancer cell line LS174T. The impact of ST3GalIV KO in the biosynthesis of SLeX isomer SLeA and non sialylated Lewis X and A were also evaluated and overall, ST3GalIV KO led to a decreased expression of SLeA and an increased expression in both LeX and LeA. In addition, the abrogation of SLeX on GI cancer cells led to a reduction in cell motility. Furthermore, ST3GalVI KO was performed in LS174T ST3GalIV KO cells, resulting in the complete abolishment of SLeX expression and consequent reduced motility capacity of those cells. Overall, these findings portray ST3GalIV as the main, but not the only, enzyme driving the biosynthesis of SLeX in GI cancer cells, with a functional impact on cancer cell motility.

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The sialyltransferase ST3Gal3 facilitates the receptivity of the uterine endometrium in vitro and in vivo

Cited by 16 publications

References 50 publications

A novel variant of ST3GAL3 causes non‐syndromic autosomal recessive intellectual disability in Iranian patients

A novel variant of ST3GAL3 causes non‐syndromic autosomal recessive intellectual disability in Iranian patients

N‐glycosylation of uterine endometrium determines its receptivity

ST3GalIV drives SLeX biosynthesis in gastrointestinal cancer cells and associates with cancer cell motility

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