{"title":"pdzk1相互作用蛋白1在结直肠癌恶性进展中的机制研究","authors":"Kuaiyun Yu, Yao Yu, Chang Zhang, Leilei Hao","doi":"10.25259/Cytojournal_200_2024","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>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.</p><p><strong>Material and methods: </strong>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.</p><p><strong>Results: </strong>PDZK1IP1 was highly expressed in the CRC tissues (<i>P</i> < 0.001) and cells (<i>P</i> < 0.05), and its knockdown restrained cell growth (<i>P</i> < 0.05), migratory potential (<i>P</i> < 0.01), and invasive capacities (<i>P</i> < 0.001) and accelerated cell apoptosis (<i>P</i> < 0.001). Mechanically, PDZK1IP1 silencing blocked CRC progression by inactivating the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of the rapamycin pathway.</p><p><strong>Conclusion: </strong>PDZK1IP1 contributes to the oncogenesis of CRC. This finding provides a basis for the diagnosis, treatment, and prevention of CRC.</p>","PeriodicalId":49082,"journal":{"name":"Cytojournal","volume":"22 ","pages":"52"},"PeriodicalIF":3.1000,"publicationDate":"2025-05-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178085/pdf/","citationCount":"0","resultStr":"{\"title\":\"Mechanistic insights into PDZK1-interacting protein 1 on the malignant progression of colorectal carcinoma.\",\"authors\":\"Kuaiyun Yu, Yao Yu, Chang Zhang, Leilei Hao\",\"doi\":\"10.25259/Cytojournal_200_2024\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>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.</p><p><strong>Material and methods: </strong>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.</p><p><strong>Results: </strong>PDZK1IP1 was highly expressed in the CRC tissues (<i>P</i> < 0.001) and cells (<i>P</i> < 0.05), and its knockdown restrained cell growth (<i>P</i> < 0.05), migratory potential (<i>P</i> < 0.01), and invasive capacities (<i>P</i> < 0.001) and accelerated cell apoptosis (<i>P</i> < 0.001). Mechanically, PDZK1IP1 silencing blocked CRC progression by inactivating the phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of the rapamycin pathway.</p><p><strong>Conclusion: </strong>PDZK1IP1 contributes to the oncogenesis of CRC. This finding provides a basis for the diagnosis, treatment, and prevention of CRC.</p>\",\"PeriodicalId\":49082,\"journal\":{\"name\":\"Cytojournal\",\"volume\":\"22 \",\"pages\":\"52\"},\"PeriodicalIF\":3.1000,\"publicationDate\":\"2025-05-10\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12178085/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cytojournal\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.25259/Cytojournal_200_2024\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2025/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q2\",\"JCRName\":\"PATHOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cytojournal","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.25259/Cytojournal_200_2024","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q2","JCRName":"PATHOLOGY","Score":null,"Total":0}
Mechanistic insights into PDZK1-interacting protein 1 on the malignant progression of colorectal carcinoma.
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 (P < 0.001) and cells (P < 0.05), and its knockdown restrained cell growth (P < 0.05), migratory potential (P < 0.01), and invasive capacities (P < 0.001) and accelerated cell apoptosis (P < 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.
期刊介绍：
The CytoJournal is an open-access peer-reviewed journal committed to publishing high-quality articles in the field of Diagnostic Cytopathology including Molecular aspects. The journal is owned by the Cytopathology Foundation and published by the Scientific Scholar.
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