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DNAJC12的抑制通过下调HSPA4表达抑制直肠癌的肿瘤发生。

Inhibition of DNAJC12 Inhibited Tumorigenesis of Rectal Cancer via Downregulating HSPA4 Expression.

作者信息

Sun Qi, Lv Yan, Sun Weihua

机构信息

Third Ward of Cancer Center, The PLA Navy Anqing Hospital, Anqing 246003, Anhui, China.

Department of Oncology, Qingdao Municipal Hospital, Qingdao 266071, Shandong, China.

出版信息

Evid Based Complement Alternat Med. 2022 Sep 21;2022:1027895. doi: 10.1155/2022/1027895. eCollection 2022.

DOI:10.1155/2022/1027895
PMID:36185081
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9519347/
Abstract

BACKGROUND

Dysregulation of DnaJ heat shock protein family (HSP40) member C12 (DNAJC12) is implicated in the malignancy progression of multiple cancers. The current study aimed to determine the biology function and mechanism of DNAJC12 in rectal cancer (RC).

METHODS

RC tissues, adjacent tissues, RC cell lines, and normal colorectal epithelial cell lines were collected to analyze DNAJC12 expression. The abilities of DNAJC12 on proliferation, migration, and apoptosis of RC cells were detected by CCK-8, wound healing, and flow cytometry assays. Co-IP assays were carried out to confirm the association between DNAJC12 and HSPA4. The effect of DNAJC12 on tumor growth was detected by using the xenograft model of nude mice.

RESULTS

Elevation of DNAJC12 was uncovered in RC tissues and cell lines. DNAJC12 upregulation facilitated RC cell proliferation and migration and induced apoptosis, while DNAJC12 interference showed the opposite results. Besides, HSAP4 served as a potential binding protein for DNAJC12. Rescue experiments revealed that elevated of HSAP4 restored the impact of DNAJC12 silencing on the cell functions. Finally, DNAJC12 silencing hampered tumor growth of RC in vivo.

CONCLUSION

In summary, this study highlighted a key player of DNAJC12 in modulating the malignant biological progression of RC via DNAJC12/HSPA4 axis, displaying a potential therapeutic target for RC.

摘要

背景

DnaJ热休克蛋白家族（HSP40）成员C12（DNAJC12）的失调与多种癌症的恶性进展有关。本研究旨在确定DNAJC12在直肠癌（RC）中的生物学功能及机制。

方法

收集RC组织、癌旁组织、RC细胞系和正常结直肠上皮细胞系，分析DNAJC12表达。通过CCK-8、伤口愈合和流式细胞术检测DNAJC12对RC细胞增殖、迁移和凋亡的影响。进行免疫共沉淀实验以证实DNAJC12与HSPA4之间的关联。利用裸鼠异种移植模型检测DNAJC12对肿瘤生长的影响。

结果

在RC组织和细胞系中发现DNAJC12升高。DNAJC12上调促进RC细胞增殖和迁移并诱导凋亡，而DNAJC12干扰则显示相反结果。此外，HSAP4是DNAJC12的潜在结合蛋白。挽救实验表明，HSAP4升高可恢复DNAJC12沉默对细胞功能的影响。最后，DNAJC12沉默在体内阻碍了RC的肿瘤生长。

结论

总之，本研究强调了DNAJC12通过DNAJC12/HSPA4轴在调节RC恶性生物学进展中的关键作用，显示出RC的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/d1997ed27f22/ECAM2022-1027895.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/4ac4a5beff7d/ECAM2022-1027895.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/9b36f8c0d17e/ECAM2022-1027895.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/2188ca8a8969/ECAM2022-1027895.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/b205267d2df7/ECAM2022-1027895.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/d1997ed27f22/ECAM2022-1027895.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/4ac4a5beff7d/ECAM2022-1027895.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/9b36f8c0d17e/ECAM2022-1027895.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/2188ca8a8969/ECAM2022-1027895.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/b205267d2df7/ECAM2022-1027895.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/89b5/9519347/d1997ed27f22/ECAM2022-1027895.005.jpg

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