NSSR1 is regulated by testosterone in the mouse uterus and extensively expressed in endometrial carcinoma

Peng, Zheng-Yu; Xiao, Ping-Jie; Yao, Qi; Zhang, Wei; Chen, Xianhua; Xu, Ping

doi:10.1007/s13277-010-0128-3

Cited by 3 publications

(2 citation statements)

References 36 publications

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“…In addition, recently we have reported that NSSR1 is also highly expressed in reproductive system, indicating the potential roles NSSR1 may play in reproduction [18]. In mouse female reproductive system, we found that NSSR1 is developmentally expressed in the uterus and extensively distributed in endometrial carcinoma [19]. In male reproductive system, our results showed that the expression of testicular NSSR1 increased significantly during mouse testes development and NSSR1 was mainly expressed in germ cells, but barely detected in sertoli cells.…”

Section: Introductionsupporting

confidence: 52%

Dephosphorylated NSSR1 Is Induced by Androgen in Mouse Epididymis and Phosphorylated NSSR1 Is Increased during Sperm Maturation

et al. 2011

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NSSR1 (Neural salient serine/arginine rich protein 1, alternatively SRp38) is a newly identified RNA splicing factor and predominantly expressed in neural tissues. Here, by Western blot analysis and immunofluorescent staining, we showed that the expression of dephosphorylated NSSR1 increased significantly during development of the caput epididymis. In adult mice, phosphorylated NSSR1 was mainly expressed in the apical side of epithelial cells, and dephosphorylated NSSR1 in caput epididymis was upregulated in a testosterone dependent manner. In addition, subcellular immunoreactive distribution of NSSR1 varied in different regions of the epididymis. With respect to the sperm, phosphorylated NSSR1 was detected in the mid-piece of the tail as well as the acrosome. Furthermore, NSSR1 was released from the sperm head during the capacitation and acrosome reaction. These findings for the first time provide the evidence for the potential roles of NSSR1 in sperm maturation and fertilization.

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Section: Introductionsupporting

confidence: 52%

Dephosphorylated NSSR1 Is Induced by Androgen in Mouse Epididymis and Phosphorylated NSSR1 Is Increased during Sperm Maturation

et al. 2011

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“…Previous studies have shown that SRSF10 is upregulated in colorectal cancer as a key regulator of BCLAF1 pre-mRNA splicing and thus maintaining the oncogenic phenotype of colon cancer cells [ 36 , 37 ]. In addition, the expression and distribution of SRSF10 are developmentally and hormonally regulated and increased in endometrial carcinomas as well as ovarian cancers, supporting its potential involvement in uterine development and tumorigenesis [ 38 ]. Here, our study infered the oncogenic role of SRSF10.…”

Section: Discussionmentioning

confidence: 99%

SRSF10-mediated IL1RAP alternative splicing regulates cervical cancer oncogenesis via mIL1RAP-NF-κB-CD47 axis

Liu

Dai

et al. 2018

Oncogene

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High-risk human papillomavirus oncoproteins E6 and E7 are the major etiological factors of cervical cancer but are insufficient for malignant transformation of cervical cancer. Dysregulated alternative splicing, mainly ascribed to aberrant splicing factor levels and activities, contributes to most cancer hallmarks. However, do E6 and E7 regulate the expression of splicing factors? Does alternative splicing acts as an “accomplice” of E6E7 to promote cervical cancer progression? Here, we identified that the splicing factor SRSF10, which promotes tumorigenesis of cervix, was upregulated by E6E7 via E2F1 transcriptional activation. SRSF10 modulates the alternate terminator of interleukin-1 receptor accessory protein exon 13 to increase production of the membrane form of interleukin-1 receptor accessory protein. SRSF10-mediated mIL1RAP upregulates the expression of the “don’t eat me” signal CD47 to inhibit macrophage phagocytosis by promoting nuclear factor-κB activation, which is pivotal in inflammatory, immune, and tumorigenesis processes. Altogether, these data reveal a close relationship among HPV infection, alternative splicing and tumor immune evasion, and also suggests that the SRSF10-mIL1RAP-CD47 axis could be an attractive therapeutic target for the treatment of cervical cancer.

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Dephosphorylation of NSSR1 regulates alternative splicing of the GluR-B minigene

Zhang

Chen

et al. 2014

Genet. Mol. Res.

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ABSTRACT. Neural salient serine/arginine-rich protein 1 (NSSR1, alternatively SRp38) is an important splicing factor that can repress pre-mRNA alternative splicing in cells during heat shock and mitosis. We show here that NSSR1 protein is dephosphorylated when cells are heat shocked or incubated with kinase inhibitor K252a. Both heat shock and K252a treatment increase the truncated splicing isoform of the GluR-B minigene pre-mRNA. We also investigated the roles of the RRM motif and three RS domains of NSSR1 in in vivo pre-mRNA splicing. The results show that deletion of the RRM motif did not affect GluR-B minigene pre-mRNA splicing, but deletion of any one of the three RS domains increases the truncated splicing isoform of the GluR-B minigene. We further show that an SRSRSK sequence in the RS3 domain may play an important role in the function of NSSR1 in pre-mRNA splicing.

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NSSR1 is regulated by testosterone in the mouse uterus and extensively expressed in endometrial carcinoma

Cited by 3 publications

References 36 publications

Dephosphorylated NSSR1 Is Induced by Androgen in Mouse Epididymis and Phosphorylated NSSR1 Is Increased during Sperm Maturation

Dephosphorylated NSSR1 Is Induced by Androgen in Mouse Epididymis and Phosphorylated NSSR1 Is Increased during Sperm Maturation

SRSF10-mediated IL1RAP alternative splicing regulates cervical cancer oncogenesis via mIL1RAP-NF-κB-CD47 axis

Dephosphorylation of NSSR1 regulates alternative splicing of the GluR-B minigene

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