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SSRPl 在癌症中的现状：困境与前路。

The Current Status of SSRP1 in Cancer: Tribulation and Road Ahead.

机构信息

Department of Respiratory Medicine, The First Hospital of Jilin University, 71 Xinmin Street, Changchun, Jilin 130021, China.

Department of Hepatopancreatobiliary Medicine, The Second Hospital of Jilin University, Changchun, China.

出版信息

J Healthc Eng. 2022 Apr 13;2022:3528786. doi: 10.1155/2022/3528786. eCollection 2022.

DOI:10.1155/2022/3528786
PMID:35463672
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9020922/
Abstract

METHODS

We search PubMed and Web of Sciences with keywords "SSRP1" and "Cancer." Only English literature was included, and conference papers and abstract were all excluded.

RESULTS

Transcription factors are classified into three groups based on their DNA binding motifs: simple helix-loop-helix (bHLH), classical zinc fingers (ZF-TFs), and homeodomains. The tumor-suppressive miR-497 (microRNA-497) acted as an undesirable regulator of SSRP1 upregulation, which led to tumor growth. The siRNA (small interfering RNA) knockdown of SSRP1 hindered cell proliferation along with incursion and glioma cell migration. Through the AKT (also known as protein kinase B) signaling pathway, SSRP1 silencing affected cancer apoptosis and cell proliferation.

CONCLUSION

The MAPK (mitogen-activated protein kinase) signaling pathway's phosphorylation was suppressed when SSRP1 was depleted. The effect of curaxins on p53 and NF-B (nuclear factor-B), and their toxicity to cancer cells, is attributable to the FACT (facilitates chromatin transcription) complex's chromatin trapping.

摘要

方法

我们使用“SSRP1”和“Cancer”作为关键词在 PubMed 和 Web of Sciences 中进行检索。仅纳入英文文献，排除会议论文和摘要。

结果

转录因子根据其 DNA 结合基序分为三类：简单螺旋-环-螺旋（bHLH）、经典锌指（ZF-TFs）和同源域。抑癌 miR-497（microRNA-497）作为 SSRP1 上调的不良调节剂，导致肿瘤生长。SSRP1 的 siRNA（小干扰 RNA）敲低抑制了细胞增殖、侵袭和神经胶质瘤细胞迁移。通过 AKT（也称为蛋白激酶 B）信号通路，SSRP1 沉默影响了癌症细胞凋亡和增殖。

结论

当 SSRP1 耗尽时，MAPK（丝裂原活化蛋白激酶）信号通路的磷酸化受到抑制。curaxins 对 p53 和 NF-B（核因子-B）的影响及其对癌细胞的毒性归因于 FACT（促进染色质转录）复合物的染色质捕获。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/a719a6d4cad7/JHE2022-3528786.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/dcde927fac2e/JHE2022-3528786.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/1d6ca74c6165/JHE2022-3528786.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/1497a54167b6/JHE2022-3528786.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/de551f13a99a/JHE2022-3528786.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/149b805bc258/JHE2022-3528786.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/a719a6d4cad7/JHE2022-3528786.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/dcde927fac2e/JHE2022-3528786.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/1d6ca74c6165/JHE2022-3528786.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/1497a54167b6/JHE2022-3528786.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/de551f13a99a/JHE2022-3528786.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/149b805bc258/JHE2022-3528786.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b21c/9020922/a719a6d4cad7/JHE2022-3528786.006.jpg

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