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螺旋-环-螺旋转录调节因子Id4是前列腺腔上皮细胞终末分化所必需的。

The helix-loop-helix transcriptional regulator Id4 is required for terminal differentiation of luminal epithelial cells in the prostate.

作者信息

Hewa Bostanthirige Dhanushka, Komaragiri Shravan K, Joshi Jugal B, Alzahrani Majid, Saini Isha, Jain Sanjay, Bowen Nathan J, Havrda Matthew C, Chaudhary Jaideep

机构信息

Center for Cancer Research and Therapeutics Development, Clark Atlanta University, Atlanta GA, USA.

Lifeline Pathology Lab and Diagnostic Center, Karnal, India.

出版信息

Oncoscience. 2021 Mar 24;8:14-30. doi: 10.18632/oncoscience.524. eCollection 2021.

DOI:10.18632/oncoscience.524
PMID:33884281
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8045964/
Abstract

Inhibitor of differentiation 4 (Id4), a member of the helix-loop-helix family of transcriptional regulators has emerged as a tumor suppressor in prostate cancer. In this study we investigated the effect of loss of Id4 () on mouse prostate development. Histological analysis was performed on prostates from 25 days, 3 months and 6 months old mice. Expression of Amacr, Ck8, Ck18, Fkbp51, Fkbp52, androgen receptor, Pten, sca-1 and Nkx3.1 was investigated by immunohistochemistry. Results were compared to the prostates from mice. mice had smaller prostates with fewer and smaller tubules. Subtle PIN like lesions were observed at 6mo. Decreased Nkx3.1 and Pten and increased stem cell marker sca-1, PIN marker Amacr and basal cell marker p63 was observed at all ages. Persistent Ck8 and Ck18 expression suggested that loss of Id4 results in epithelial commitment but not terminal differentiation in spite of active Ar. Loss of Id4 attenuates normal prostate development and promotes hyperplasia/ dysplasia with PIN like lesions. The results suggest that loss of Id4 maintains stem cell phenotype of "luminal committed basal cells", identifying a unique prostate developmental pathway regulated by Id4.

摘要

分化抑制因子4（Id4）是转录调节因子螺旋-环-螺旋家族的成员，已成为前列腺癌中的一种肿瘤抑制因子。在本研究中，我们调查了Id4缺失对小鼠前列腺发育的影响。对25天、3个月和6个月大的小鼠前列腺进行了组织学分析。通过免疫组织化学研究了Amacr、Ck8、Ck18、Fkbp51、Fkbp52、雄激素受体、Pten、sca-1和Nkx3.1的表达。将结果与野生型小鼠的前列腺进行比较。Id4缺失的小鼠前列腺较小，小管数量减少且管径变小。在6个月时观察到轻微的PIN样病变。在所有年龄段均观察到Nkx3.1和Pten减少，干细胞标志物sca-1、PIN标志物Amacr和基底细胞标志物p63增加。持续的Ck8和Ck18表达表明，尽管雄激素受体（Ar）活跃，但Id4缺失导致上皮定向分化而非终末分化。Id4缺失会减弱正常前列腺发育，并促进伴有PIN样病变的增生/发育异常。结果表明，Id4缺失维持了“管腔定向基底细胞”的干细胞表型，确定了一条由Id4调节的独特前列腺发育途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/fe831b10964d/oncoscience-08-14-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/b017c4d4d0a1/oncoscience-08-14-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/9100980e018d/oncoscience-08-14-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/2e8137dc35ee/oncoscience-08-14-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/703bc8082f94/oncoscience-08-14-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/e09267ac8734/oncoscience-08-14-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/2757812bee7d/oncoscience-08-14-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/51e701175425/oncoscience-08-14-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/7bdc9e2fd8d6/oncoscience-08-14-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/fe831b10964d/oncoscience-08-14-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/b017c4d4d0a1/oncoscience-08-14-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/9100980e018d/oncoscience-08-14-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/2e8137dc35ee/oncoscience-08-14-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/703bc8082f94/oncoscience-08-14-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/e09267ac8734/oncoscience-08-14-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/2757812bee7d/oncoscience-08-14-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/51e701175425/oncoscience-08-14-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/7bdc9e2fd8d6/oncoscience-08-14-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/659d/8045964/fe831b10964d/oncoscience-08-14-g009.jpg

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本文引用的文献

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Prostate Luminal Progenitor Cells in Development and Cancer.发育和癌症中的前列腺管腔祖细胞
Trends Cancer. 2018 Nov;4(11):769-783. doi: 10.1016/j.trecan.2018.09.003. Epub 2018 Oct 1.
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Clinical implications of PTEN loss in prostate cancer.PTEN 缺失在前列腺癌中的临床意义。
Nat Rev Urol. 2018 Apr;15(4):222-234. doi: 10.1038/nrurol.2018.9. Epub 2018 Feb 20.
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Inactivation of ID4 promotes a CRPC phenotype with constitutive AR activation through FKBP52.ID4 的失活通过 FKBP52 促进了具有持续 AR 激活的 CRPC 表型。
Mol Oncol. 2017 Apr;11(4):337-357. doi: 10.1002/1878-0261.12028. Epub 2017 Mar 2.
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ID4 regulates transcriptional activity of wild type and mutant p53 via K373 acetylation.ID4通过K373乙酰化调节野生型和突变型p53的转录活性。
Oncotarget. 2017 Jan 10;8(2):2536-2549. doi: 10.18632/oncotarget.13701.
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Inhibitor of differentiation 4 (ID4): From development to cancer.分化抑制因子4（ID4）：从发育到癌症
Biochim Biophys Acta. 2015 Jan;1855(1):92-103. doi: 10.1016/j.bbcan.2014.12.002. Epub 2014 Dec 12.
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Inhibitor of differentiation 4 (ID4) inactivation promotes de novo steroidogenesis and castration-resistant prostate cancer.分化抑制因子4（ID4）失活促进前列腺癌去势抵抗及新的类固醇生成。
Mol Endocrinol. 2014 Aug;28(8):1239-53. doi: 10.1210/me.2014-1100. Epub 2014 Jun 12.
7
Id4 deficiency attenuates prostate development and promotes PIN-like lesions by regulating androgen receptor activity and expression of NKX3.1 and PTEN.Id4基因缺陷通过调节雄激素受体活性以及NKX3.1和PTEN的表达，减弱前列腺发育并促进前列腺上皮内瘤样病变。
Mol Cancer. 2013 Jun 21;12:67. doi: 10.1186/1476-4598-12-67.
8
Epigenetic inactivation of inhibitor of differentiation 4 (Id4) correlates with prostate cancer.抑瘤分化因子 4（Id4）的表观遗传失活与前列腺癌相关。
Cancer Med. 2012 Oct;1(2):176-86. doi: 10.1002/cam4.16. Epub 2012 Aug 2.
9
Cooperation between Polycomb and androgen receptor during oncogenic transformation.多梳抑制复合物和雄激素受体在致癌转化过程中的合作。
Genome Res. 2012 Feb;22(2):322-31. doi: 10.1101/gr.131508.111. Epub 2011 Dec 16.
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