摘要：
Nasopharyngeal carcinoma (NPC) is an aggressive head and neck tumor that is influenced by a variety of molecular factors during its pathogenesis. Among these, the phosphatase and tensin homolog (PTEN) plays a crucial role in regulatory networks. This article systematically reviews the multifaceted functions of PTEN in NPC, including its roles in inhibiting cell proliferation, regulating migration and invasion, promoting autophagy and apoptosis, and influencing resistance to radiotherapy. Molecular factors such as long non-coding RNA, microRNA (miRNA), and circular RNA can modulate PTEN through various pathways, thereby impacting the biological behavior of NPC. In addition, PTEN is involved in regulating the tumor microenvironment of NPC, and its interaction with the Epstein-Barr virus has also recently become a focus of research. A comprehensive understanding of the PTEN regulatory network provides a foundation for future personalized and targeted therapeutic strategies. This study expands our understanding of the pathogenesis of NPC and suggests new directions in the field of tumor biology and NPC treatment.
摘要：
Chemical carcinogen is one etiology of nasopharyngeal carcinoma (NPC) occurrence, N,N'Dinitrosopiperazine (DNP) has been verified to cause NPC cell metastasis and generate induced pluripotent stem cells (iPSCs). To investigate the oncogenic mechanism of DNP, NPC cells were exposed to DNP, and subjected to RNA-seq, GRO-seq, ChIP-seq, and data analysis. The results showed that the super-enhancer RNA (seRNA) participates in DNP-mediated NPC metastasis through regulating N-myc downstream regulated gene 1 (NDRG1). Mechanistically, DNP exposure upregulates the levels of NPC metastatic seRNA (seRNA-NPCm), seRNA-NPCm interacted with a special super-enhancer (SE) upstream of NDRG1 gene and bound to nucleophosmin (NPM1)/c-Myc complex at the NDRG1 promoter, resulting in an increase of NDRG1 transcription. Functional studies showed that DNP significantly increased the metastatic capability of NPC cells in vitro and in vivo. Knockdown of seRNA-NPCm in NPC cells impaired the capability of metastasis. Furthermore, stably overexpressing seRNA-NPCm significantly increased the metastatic ability of NPC cells, while restoration of NDRG1 levels in these cells restored their metastatic capacity. Finally, the immunohistochemistry and in situ hybridization analyses revealed that the expression of seRNA-NPCm in NPC patients is positively correlated with NDRG1, and the NDRG1 level independently predicts poor prognosis of NPC patients. Collectively, DNP induces seRNA-NPCm, and seRNA-NPCm promotes NPC metastasis through NPM1/c-Myc/NDRG1 axis.
作者机构：
College of Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China;[蔺婷; 胡晶] Hunan Provincial Engineering and Technological Research Center for Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Chinese Medicine and Protecting Visual Function, Changsha, 410208, China;[何迎春; 周芳亮; 胡梅] College of Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China, Hunan Provincial Engineering and Technological Research Center for Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Chinese Medicine and Protecting Visual Function, Changsha, 410208, China
通讯机构：
[He, Y.-C.] C;College of Medicine, Hunan University of Chinese Medicine, Changsha, China
摘要：
Herein, we investigated the effects of combining berberine (Ber; the major active constituent of Rhizoma coptidis) with ginsenoside Rg3 (Rg3; an active ingredient of Panax ginseng) on the proliferation and apoptosis of nasopharyngeal carcinoma (NPC) cells, and explored the underlying mechanism. Combining Ber with Rg3 synergistically inhibited the proliferation of NPC CNE2 cells in vitro and in vivo. Additionally, Ber combined with Rg3 induced apoptosis by promoting the expression of apoptosis-related protein Box, and inhibiting the expression of Survivin, PCNA and anti-apoptotic protein Bcl-2. Ber combined with Rg3 plays a role in anti-NPC through MAPK/ERK pathway. Ber combined with Rg3 is a potent natural combination agent with potential for treating and preventing NPC.
摘要：
缺血-再灌注(ischemia-reperfusion,I/R)损伤是指在脏器缺血的基础上恢复血流,不仅未能使脏器原来的功能恢复,反而使功能进一步受损.目前临床上发现有很多脏器组织存在缺血-再灌注损伤现象,其中报道最多的在心肌、脑组织、肝脏、肾脏等,其主要改变发生在组织超微结构、能量代谢和电生理等一系列损伤性变化.研究发现,从黄连中提取的黄连素可通过多种作用机制对损伤器官产生保护或逆转作用,其机制主要与调控PTEN/Akt信号通路、JAK2/STAT3/NF-KB信号通路、Notch1/Hes1-PTEN/Akt信号通路、PI3K/Akt/mTOR(哺乳动物雷帕霉素靶蛋白manmalian target of rapamycin,mTOR)信号通路等密切相关.
作者机构：
Post-Graduate School, Hunan University of Chinese Medicine, Changsha, 410208, China;Hunan Provincial Key Lab for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China;[胡梅] College of Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China;Hunan Provincial Research Engineering Technology Center for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Traditional Chinese Medicine and Visual Function Protection, Hunan University of Chinese Medicine, Changsha, 410208, China;College of traditional Chinese Medicine, Changsha Medical University, Changsha, 410219, China
通讯机构：
[He, Y.] H;Hunan Provincial Key Lab for the Prevention and Treatment of Ophthalmology and Otolaryngology Diseases with Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, China
关键词：
益气解毒方;鼻咽癌;细胞凋亡;MAPK/ERK信号通路
摘要：
目的 研究益气解毒方水提物对鼻咽癌细胞凋亡的影响,并从MAPK/ERK信号通路探讨其诱导凋亡的作用机制。方法 CCK-8法检测益气解毒方水提物对CNE1、CNE2细胞增殖的影响;Hoechst 33342染色法、JC-10染色法、荧光双染流式细胞仪检测其对CNE1、CNE2细胞凋亡的影响;Western blot法检测其对CNE1、CNE2细胞蛋白表达的影响。结果 益气解毒方水提物能抑制CNE1、CNE2细胞增殖( P <0.05)、诱导凋亡( P <0.05);药物作用48 h后,Survivin、XIAP、Bcl-2表达下降,Bax表达上升,MAPK/ERK信号通路关键蛋白p-c-Raf、p-MEK、p-ERK表达下降( P <0.05);在此基础上,加入激活剂ISO和益气解毒方水提物后,与单用益气解毒方水提物相比,p-c-Raf、p-MEK、p-ERK1/2表达上调,Survivin、XIAP、Bcl-2表达增加,Bax表达下降,促凋亡效应也降低( P <0.05)。结论 益气解毒方水提物可诱导鼻咽癌细胞凋亡,该效应与其抑制MAPK/ERK信号通路关键蛋白p-c-Raf、p-MEK、p-ERK1/2表达,进而下调Survivin、XIAP、Bcl-2表达,上调Bax表达有关。
