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PDZK1相互作用蛋白1对结直肠癌恶性进展的机制性见解

Mechanistic insights into PDZK1-interacting protein 1 on the malignant progression of colorectal carcinoma.

作者信息

Yu Kuaiyun, Yu Yao, Zhang Chang, Hao Leilei

机构信息

Department of General Surgery, Yantaishan Hospital, Yantai, Shandong Province, China.

Department of General Pediatric Surgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, Shandong Province, China.

出版信息

Cytojournal. 2025 May 10;22:52. doi: 10.25259/Cytojournal_200_2024. eCollection 2025.

Abstract

OBJECTIVE

PDZ domain containing 1-interacting protein 1 (PDZK1IP1) is commonly overexpressed in a wide variety of cancer. Hence, the objective of the present study is to ascertain the influences of PDZK1IP1 on colorectal carcinoma (CRC) development.

MATERIAL AND METHODS

PDZK1IP1 expression was tested through reverse transcription-quantitative polymerase chain reaction and Western blot analysis, and its correlation with prognosis was analyzed using the GEPIA website. Small interfering RNA against PDZK1IP1 was adopted to downregulate PDZK1IP1 expression in CRC cells. The effects of PDZK1IP1 on cell growth were ascertained using colony formation and CCK-8 tests, and CRC cell apoptosis was analyzed through flow cytometry. Cell migration capability and invasiveness were measured using Matrigel Transwell and scratch-healing assays.

RESULTS

PDZK1IP1 was highly expressed in the CRC tissues ( < 0.001) and cells ( < 0.05), and its knockdown restrained cell growth ( < 0.05), migratory potential ( < 0.01), and invasive capacities ( < 0.001) and accelerated cell apoptosis ( < 0.001). Mechanically, PDZK1IP1 silencing blocked CRC progression by inactivating the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of the rapamycin pathway.

CONCLUSION

PDZK1IP1 contributes to the oncogenesis of CRC. This finding provides a basis for the diagnosis, treatment, and prevention of CRC.

摘要

目的

含PDZ结构域的1相互作用蛋白1(PDZK1IP1)在多种癌症中普遍过表达。因此,本研究的目的是确定PDZK1IP1对结直肠癌(CRC)发生发展的影响。

材料与方法

通过逆转录定量聚合酶链反应和蛋白质免疫印迹分析检测PDZK1IP1的表达,并使用GEPIA网站分析其与预后的相关性。采用针对PDZK1IP1的小干扰RNA下调CRC细胞中PDZK1IP1的表达。使用集落形成试验和CCK-8试验确定PDZK1IP1对细胞生长的影响,并通过流式细胞术分析CRC细胞凋亡。使用基质胶Transwell试验和划痕愈合试验测量细胞迁移能力和侵袭性。

结果

PDZK1IP1在CRC组织(<0.001)和细胞(<0.05)中高表达,其敲低抑制细胞生长(<0.05)、迁移潜能(<0.01)和侵袭能力(<0.001),并加速细胞凋亡(<0.001)。机制上,PDZK1IP1沉默通过使磷脂酰肌醇3激酶/蛋白激酶B/雷帕霉素机制靶点通路失活来阻断CRC进展。

结论

PDZK1IP1促进CRC的肿瘤发生。这一发现为CRC的诊断、治疗和预防提供了依据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c99d/12178085/2466f90c4510/Cytojournal-22-52-g001.jpg

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