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2023年7月，黑龍江省科學(xué)院先進(jìn)技術(shù)研究所;黑龍江省科學(xué)院先進(jìn)技術(shù)研究所(Institute of Advanced Technology, Heilongjiang Academy of Sciences；Institute of Advanced Technology, Heilongjiang Academy of Sciences) Guoqing Huang老師研究團(tuán)隊(duì)在《Research Square》上發(fā)表論文：
“The effect of DDIT3 on luminal A type breast cancer"
“DDIT3對(duì)Luminal A型乳腺癌的影響"
Abstract：
Purpose: To analyze the phenotypic changes of breast cancer (BC) cell before and after DDIT3 knockdown/overexpression, and preliminarily explore the regulatory mechanism. Also, to analyze the relationship between DDIT3 and prognosis by combining with bioinformatics methods, which provide a basis for further research on DDIT3 targeted treatment of BC.
Methods: Loss- and gain-of-function studies, DDIT3 in MCF-7 (luminal A), and RNA-seq analysis were employed to investigate the functional impact of DDIT3 on BC cell proliferation and drug resistance. The relationship between DDIT3 and the prognosis of BC patients was systematically assessed using the tissue microarray technique along with qRT-PCR and publicly available data.
Results: Survival analysis showed that patients with lower DDIT3 expression in luminal A type BC or BC patient which were undergoing endocrine therapy had a poorer prognosis, and DDIT3 expression was associated with overall survival (OS) significant. Following the knockdown of DDIT3 in MCF-7 cells, the proliferation rate was significantly increased, and drug resistance ability was just reversed. On the contrary, overexpression of DDIT3 had a relative inhibitory effect on target cell proliferation. Notably, the inhibition of DDIT3 expression upregulated TP63 and downregulated PDGFR, with the results being exactly opposite after the overexpression of DDIT3.
Conclusion: These results have revealed that DDIT3 plays a critical role in luminal A type BC cell proliferation and TAM resistance, and it holds potential prognostic value in BC. Overall, DDIT3 may exert its functions in luminal A type BC by modulating the expression of TP63 and PDGFR.
摘要：
目的:分析乳腺癌(BC)細(xì)胞DDIT3敲低/過(guò)表達(dá)前后的表型變化，并初步探討其調(diào)控機(jī)制。結(jié)合生物信息學(xué)方法分析DDIT3與預(yù)后的關(guān)系，為進(jìn)一步研究DDIT3靶向治療BC提供依據(jù)。
方法:通過(guò)功能缺失和功能獲得研究、MCF-7 (luminal A)中的DDIT3和RNA-seq分析來(lái)研究DDIT3對(duì)BC細(xì)胞增殖和耐藥的功能影響。利用組織微陣列技術(shù)、qRT-PCR和公開(kāi)數(shù)據(jù)系統(tǒng)評(píng)估DDIT3與BC患者預(yù)后的關(guān)系。
結(jié)果:生存分析顯示，在Luminal A BC或接受內(nèi)分泌治療的BC患者中，DDIT3表達(dá)較低的患者預(yù)后較差，且DDIT3表達(dá)與總生存(OS)顯著相關(guān)。MCF-7細(xì)胞中敲低DDIT3后，增殖速率明顯提高，耐藥能力剛好逆轉(zhuǎn)。相反，過(guò)表達(dá)DDIT3對(duì)靶細(xì)胞增殖有相對(duì)抑制作用。值得注意的是，抑制DDIT3表達(dá)可上調(diào)TP63，下調(diào)PDGFR，而過(guò)表達(dá)DDIT3后的結(jié)果正好相反。
結(jié)論:這些結(jié)果揭示了DDIT3在Luminal A BC細(xì)胞增殖和TAM耐藥中起關(guān)鍵作用，并具有潛在的預(yù)后價(jià)值。綜上所述，dddit3可能通過(guò)調(diào)節(jié)TP63和PDGFR的表達(dá)而在luminal A型BC中發(fā)揮作用。
該論文中，HEK293T和人乳腺癌(BC)細(xì)胞系MCF-7的體外培養(yǎng)是使用Ausbian特級(jí)胎牛血清完成的。
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