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【佳學(xué)基因檢測(cè)】抗血小板治療增加分泌型 SERPINE1 表達(dá),誘導(dǎo) MMP1 表達(dá)和增加結(jié)腸癌轉(zhuǎn)移

參加學(xué)術(shù)會(huì)議時(shí)獲悉《Int J Mol Sci》在.?2022 Aug 24;23(17):9596.發(fā)表了一篇題目為《抗血小板治療增加分泌型 SERPINE1 表達(dá),誘導(dǎo) MMP1 表達(dá)和增加結(jié)腸癌轉(zhuǎn)移》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Won-Tae Kim,?Jeong-Yeon Mun,?Seung-Woo Baek,?Min-Hye Kim,?Gi-Eun Yang,?Mi-So Jeong,?Sun Young Choi,?Jin-Yeong Han,?Moo Hyun Kim,?Sun-Hee Leem等完成。促進(jìn)了腫瘤的正確治療與個(gè)性化用藥的發(fā)展,進(jìn)一步強(qiáng)調(diào)了基因信息檢測(cè)與分析的重要性。

佳學(xué)基因檢測(cè)】抗血小板治療增加分泌型 SERPINE1 表達(dá),誘導(dǎo) MMP1 表達(dá)和增加結(jié)腸癌轉(zhuǎn)移

基因檢測(cè)多少錢一次—共識(shí)


參加學(xué)術(shù)會(huì)議時(shí)獲悉《Int J Mol Sci》在.?2022 Aug 24;23(17):9596.發(fā)表了一篇題目為《抗血小板治療增加分泌型 SERPINE1 表達(dá),誘導(dǎo) MMP1 表達(dá)和增加結(jié)腸癌轉(zhuǎn)移》腫瘤靶向藥物治療基因檢測(cè)臨床研究文章。該研究由Won-Tae Kim,?Jeong-Yeon Mun,?Seung-Woo Baek,?Min-Hye Kim,?Gi-Eun Yang,?Mi-So Jeong,?Sun Young Choi,?Jin-Yeong Han,?Moo Hyun Kim,?Sun-Hee Leem等完成。促進(jìn)了腫瘤的正確治療與個(gè)性化用藥的發(fā)展,進(jìn)一步強(qiáng)調(diào)了基因信息檢測(cè)與分析的重要性。


腫瘤靶向藥物及正確治療臨床研究?jī)?nèi)容關(guān)鍵詞:


MMP1,絲氨酸1,抗血小板藥物,癌癥轉(zhuǎn)移


腫瘤靶向治療基因檢測(cè)臨床應(yīng)用結(jié)果


與許多關(guān)于抗血小板藥物抑制癌癥生長(zhǎng)和轉(zhuǎn)移的報(bào)道相反,在接受長(zhǎng)期抗血小板治療的患者中報(bào)告了新的實(shí)體瘤。我們研究了這些藥物在沒有血小板的情況下直接對(duì)癌細(xì)胞的影響,以模擬長(zhǎng)期治療的效果。當(dāng)將四種抗血小板藥物(阿司匹林、氯吡格雷、普拉格雷和替格瑞洛)用于結(jié)腸癌細(xì)胞時(shí),癌細(xì)胞增殖受到抑制,與之前的研究相似。然而,令人驚訝的是,當(dāng)用嘌呤能 P2Y12 抑制劑(嘌呤能抗血小板劑)處理細(xì)胞時(shí),癌細(xì)胞的運(yùn)動(dòng)性顯著增加。因此,確定了基因表達(dá)譜以研究 P2Y12 抑制劑對(duì)細(xì)胞遷移率的影響,并且 Serpin 家族 1 (SERPINE1) 被確定為與三組細(xì)胞遷移和細(xì)胞死亡相關(guān)的常見基因。抗血小板治療增加了癌細(xì)胞中 SERPINE1 的水平,也促進(jìn)了 SERPINE1 分泌到培養(yǎng)基中。發(fā)現(xiàn)增加的 SERPINE1 可誘導(dǎo) MMP1,從而增加細(xì)胞運(yùn)動(dòng)性。此外,使用接受這些抗血小板藥物的患者的血清證實(shí)了 SERPINE1 的增加。基于這些結(jié)果,我們提出SERPINE1可以作為一個(gè)新的靶基因,在長(zhǎng)期抗血小板治療的患者中預(yù)防癌癥的發(fā)生和轉(zhuǎn)移。絲氨酸1;抗血小板藥物;癌癥轉(zhuǎn)移。


腫瘤發(fā)生與反復(fù)轉(zhuǎn)移國(guó)際數(shù)據(jù)庫(kù)描述:


Contrary to many reports that antiplatelet agents inhibit cancer growth and metastasis, new solid tumors have been reported in patients receiving long-term antiplatelet therapy. We investigated the effects of these agents directly on cancer cells in the absence of platelets to mimic the effects of long-term therapy. When four antiplatelet agents (aspirin, clopidogrel, prasugrel, and ticagrelor) were administered to colon cancer cells, cancer cell proliferation was inhibited similarly to a previous study. However, surprisingly, when cells were treated with a purinergic P2Y12 inhibitor (purinergic antiplatelet agent), the motility of the cancer cells was significantly increased. Therefore, gene expression profiles were identified to investigate the effect of P2Y12 inhibitors on cell mobility, and Serpin family 1 (SERPINE1) was identified as a common gene associated with cell migration and cell death in three groups. Antiplatelet treatment increased the level of SERPINE1 in cancer cells and also promoted the secretion of SERPINE1 into the medium. Increased SERPINE1 was found to induce MMP1 and, thus, increase cell motility. In addition, an increase in SERPINE1 was confirmed using the serum of patients who received these antiplatelet drugs. With these results, we propose that SERPINE1 could be used as a new target gene to prevent the onset and metastasis of cancer in patients with long-term antiplatelet therapy.Keywords:?MMP1; SERPINE1; antiplatelet agents; cancer metastasis.



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