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解析上皮-间质转化(EMT)在结直肠癌中的作用:转移、治疗反应及重新审视分子途径

Unraveling the function of epithelial-mesenchymal transition (EMT) in colorectal cancer: Metastasis, therapy response, and revisiting molecular pathways.

作者信息

Sabouni Eisa, Nejad Melina Maghsodlou, Mojtabavi Sarah, Khoshduz Sara, Mojtabavi Mahsa, Nadafzadeh Niloufar, Nikpanjeh Negin, Mirzaei Sepideh, Hashemi Mehrdad, Aref Amir Reza, Khorrami Ramin, Nabavi Noushin, Ertas Yavuz Nuri, Salimimoghadam Shokooh, Zandieh Mohammad Arad, Rahmanian Parham, Taheriazam Afshin, Hushmandi Kiavash

机构信息

Faculty of Veterinary Medicine, Islamic Azad University, Science and Research Branch, Tehran, Iran.

Faculty of Medicine, Guilan University of Medical Sciences, Rasht, Iran.

出版信息

Biomed Pharmacother. 2023 Apr;160:114395. doi: 10.1016/j.biopha.2023.114395. Epub 2023 Feb 15.

DOI:10.1016/j.biopha.2023.114395
PMID:36804124
Abstract

Colorectal cancer (CRC) is a dangerous form of cancer that affects the gastrointestinal tract. It is a major global health concern, and the aggressive behavior of tumor cells makes it difficult to treat, leading to poor survival rates for patients. One major challenge in treating CRC is the metastasis, or spread, of the cancer, which is a major cause of death. In order to improve the prognosis for patients with CRC, it is necessary to focus on ways to inhibit the cancer's ability to invade and spread. Epithelial-mesenchymal transition (EMT) is a process that is linked to the spread of cancer cells, also known as metastasis. The process transforms epithelial cells into mesenchymal ones, increasing their mobility and ability to invade other tissues. This has been shown to be a key mechanism in the progression of colorectal cancer (CRC), a particularly aggressive form of gastrointestinal cancer. The activation of EMT leads to increases in the spread of CRC cells, and during this process, levels of the protein E-cadherin decrease while levels of N-cadherin and vimentin increase. EMT also contributes to the development of resistance to chemotherapy and radiation therapy in CRC. Non-coding RNAs, such as long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), play a role in regulating EMT in CRC, often through their ability to "sponge" microRNAs. Anti-cancer agents have been shown to suppress EMT and reduce the progression and spread of CRC cells. These findings suggest that targeting EMT or related mechanisms may be a promising approach for treating CRC patients in the clinic.

摘要

结直肠癌(CRC)是一种影响胃肠道的危险癌症形式。它是全球主要的健康问题,肿瘤细胞的侵袭性使其难以治疗,导致患者生存率较低。治疗CRC的一个主要挑战是癌症的转移,即扩散,这是主要的死亡原因。为了改善CRC患者的预后,有必要关注抑制癌症侵袭和扩散能力的方法。上皮-间质转化(EMT)是一个与癌细胞扩散(也称为转移)相关的过程。该过程将上皮细胞转化为间充质细胞,增加其迁移能力和侵袭其他组织的能力。这已被证明是结直肠癌(CRC)进展的关键机制,CRC是一种特别侵袭性的胃肠道癌症形式。EMT的激活导致CRC细胞扩散增加,在此过程中,E-钙黏蛋白水平降低,而N-钙黏蛋白和波形蛋白水平升高。EMT也有助于CRC对化疗和放疗产生耐药性。非编码RNA,如长链非编码RNA(lncRNA)和环状RNA(circRNA),通常通过其“吸附”微小RNA的能力在调节CRC中的EMT中发挥作用。抗癌药物已被证明可抑制EMT并减少CRC细胞的进展和扩散。这些发现表明,针对EMT或相关机制可能是临床上治疗CRC患者的一种有前景的方法。

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