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SDR16C5促进胰腺癌的增殖和迁移并抑制其凋亡。

SDR16C5 promotes proliferation and migration and inhibits apoptosis in pancreatic cancer.

作者信息

Hong Kunqiao, Yang Qian, Yin Haisen, Zhang Jianwei, Yu Baoping

机构信息

Department of Gastroenterology, Key Laboratory of Hubei Province for Digestive System Disease, Renmin Hospital of Wuhan University, Wuhan, China.

Department of Gastroenterology, Guizhou Provincial People's Hospital, Guiyang City, Guizhou Province, China.

出版信息

Open Life Sci. 2023 Jun 20;18(1):20220630. doi: 10.1515/biol-2022-0630. eCollection 2023.

DOI:10.1515/biol-2022-0630
PMID:37360782
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10290281/
Abstract

Pancreatic cancer (PAAD) is usually found when it is already in its advanced stage, which has limited options available for treatment and poor overall survival. The SDR16C5 gene is necessary for embryonic and adult tissue differentiation, development, and apoptosis, and it also participates in immune response and regulates energy metabolism. However, the role of SDR16C5 in PAAD remains unclear. In this study, we find that SDR16C5 was highly expressed in multiple tumors including PAAD. Furthermore, higher expression of SDR16C5 was significantly associated with poorer survival. We also find that the knockdown of SDR16C5 can inhibit PAAD cell proliferation and promote cell apoptosis by repressing Bcl-2, cleaved caspase 3, and cleaved caspase 9 protein expression. Moreover, silencing SDR16C5 inhibits the migration of PANC-1 and SW1990 cells by interrupting epithelial-mesenchymal transition. KEGG pathway analysis and immunofluorescence staining indicate that SDR16C5 is associated with immunity and may also participate in the development of PAAD through the IL-17 signaling pathway. Collectively, our findings provide evidence that SDR16C5 is overexpressed in PAAD patients and promotes its proliferation, migration, invasion, and apoptosis-inhibition of PAAD cells. Thus, SDR16C5 may be a potential prognostic and therapeutic target.

摘要

胰腺癌(PAAD)通常在已处于晚期时才被发现,此时治疗选择有限且总体生存率较低。SDR16C5基因对于胚胎和成人组织的分化、发育及凋亡是必需的,它还参与免疫反应并调节能量代谢。然而,SDR16C5在PAAD中的作用仍不清楚。在本研究中,我们发现SDR16C5在包括PAAD在内的多种肿瘤中高表达。此外,SDR16C5的高表达与较差的生存率显著相关。我们还发现,敲低SDR16C5可通过抑制Bcl-2、裂解的caspase 3和裂解的caspase 9蛋白表达来抑制PAAD细胞增殖并促进细胞凋亡。此外,沉默SDR16C5可通过中断上皮-间质转化来抑制PANC-1和SW1990细胞的迁移。KEGG通路分析和免疫荧光染色表明,SDR16C5与免疫相关,并且可能还通过IL-17信号通路参与PAAD的发生发展。总体而言,我们的研究结果表明,SDR16C5在PAAD患者中过表达,并促进PAAD细胞的增殖、迁移、侵袭及凋亡抑制。因此,SDR16C5可能是一个潜在的预后和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/6d44854f1369/j_biol-2022-0630-fig010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/c4eec4ee82c3/j_biol-2022-0630-ga001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/4bc371f94b64/j_biol-2022-0630-fig001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/7bf54c39042c/j_biol-2022-0630-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/c2ed99a6bb29/j_biol-2022-0630-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/0cf708ce41fb/j_biol-2022-0630-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/c33df939f80b/j_biol-2022-0630-fig006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/18248e0c3ebd/j_biol-2022-0630-fig007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/928f378c2920/j_biol-2022-0630-fig008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/59154e8f0a72/j_biol-2022-0630-fig009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/6d44854f1369/j_biol-2022-0630-fig010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/c4eec4ee82c3/j_biol-2022-0630-ga001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/4bc371f94b64/j_biol-2022-0630-fig001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/cd790bfa2d2d/j_biol-2022-0630-fig002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/7bf54c39042c/j_biol-2022-0630-fig003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/c2ed99a6bb29/j_biol-2022-0630-fig004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/0cf708ce41fb/j_biol-2022-0630-fig005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/c33df939f80b/j_biol-2022-0630-fig006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/18248e0c3ebd/j_biol-2022-0630-fig007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/928f378c2920/j_biol-2022-0630-fig008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/59154e8f0a72/j_biol-2022-0630-fig009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f4c/10290281/6d44854f1369/j_biol-2022-0630-fig010.jpg

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