scholarly journals Non-coding RNAs in necroptosis, pyroptosis and ferroptosis in cancer metastasis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yan Liu ◽  
Qiuyun Chen ◽  
Yanan Zhu ◽  
Tiying Wang ◽  
Lijuan Ye ◽  
...  

AbstractDistant metastasis is the main cause of death for cancer patients. Recently, the newly discovered programmed cell death includes necroptosis, pyroptosis, and ferroptosis, which possesses an important role in the process of tumor metastasis. At the same time, it is widely reported that non-coding RNA precisely regulates programmed death and tumor metastasis. In the present review, we summarize the function and role of necroptosis, pyrolysis, and ferroptosis involving in cancer metastasis, as well as the regulatory factors, including non-coding RNAs, of necroptosis, pyroptosis, and ferroptosis in the process of tumor metastasis.

2019 ◽  
Vol 19 (4) ◽  
pp. 277 ◽  
Author(s):  
Malika Al-Dughaishi ◽  
Asem Shalaby ◽  
Khawla Al-Ribkhi ◽  
Ammar Boudaka ◽  
Mohamed-Rachid Boulassel ◽  
...  

Programmed death ligand 1 (PD-L1) is an inhibitory molecule expressed by cancer cells to supress T-cell activity and escape anti-tumour immunity. The role of PD-L1 in cancer has been studied extensively as it is considered an important immune checkpoint against immune over-activation through its interaction with Programmed death receptor 1 (PD-1) expressed on activated lymphocytes. PD-L1 expression was found to be enhanced by chemotherapy through different proliferation pathways. However, the predictive and prognostic value for PD-L1 expression in cancer patients treated with neoadjuvant chemotherapy (NAC) is not yet established. This review focused on the potential effects of chemotherapy on PD-L1 expression and the role of PD-L1 as a prognostic and predictive marker in NAC-treated cancer patients. In addition, the potential use of this marker in clinical practice is discussed.Keywords: Programmed Cell Death 1 Ligand 1; Programmed Cell Death 1 Receptor; Neoadjuvant Therapy; Cancer.


2019 ◽  
Vol 9 ◽  
Author(s):  
Mengxiang Zhao ◽  
Nisha Zhu ◽  
Fengyao Hao ◽  
Yuxian Song ◽  
Zhiyong Wang ◽  
...  

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7433 ◽  
Author(s):  
Jiasi Wang ◽  
Yanpeng Chu ◽  
Jie Li ◽  
Tingjie Wang ◽  
Liangli Sun ◽  
...  

Background Carcinoembryonic antigen (CEA) as a diagnostic or prognostic marker has been widely studied in patients with lung cancer. However, the relationship between serum CEA and tumor metastasis in lung cancer remains controversial. This study aimed to investigate the ability of serum CEA to assess tumor metastasis in lung cancer patients. Methods We performed a retrospective analysis of 238 patients diagnosed with lung cancer from January to December 2016 at pneumology department of Dazhou Central Hospital (Dazhou, China). Serum CEA levels were quantified in each patient at the time of diagnosis of lung cancer. Metastasis was confirmed by computed tomography (CT), and/or positron emission tomography (PET) and/or surgery or other necessary detecting methods. Results Of the 213 patients eligible for final analysis, 128 were diagnosed with metastasis and 85 were diagnosed without metastasis. Compared to non-metastatic patients, the serum CEA was markedly higher in patients with metastasis (p < 0.001), and the area under the curve (AUC) was 0.724 (95% CI [0.654–0.793]). Subsequent analyses regarding the number and location of tumor metastases showed that CEA also had clinical value for multiple metastases versus single metastasis (AUC = 0.780, 95% CI [0.699–0.862]) and distant metastasis versus non-distant metastasis (AUC = 0.815, 95% CI [0.733–0.897]). In addition, we found that tumor size, histology diagnosis, age and gender had no impact on the assessment performance of CEA. Conclusion Our study suggested the serum CEA as a valuable marker for tumor metastases assessment in newly diagnosed lung cancer patients, which could have some implications in clinical application.


2021 ◽  
Vol 12 (9) ◽  
Author(s):  
Bo Sun ◽  
Fang-Jing Zhong ◽  
Cong Xu ◽  
Yi-Ming Li ◽  
Yan-Rong Zhao ◽  
...  

AbstractTumour metastasis is the main cause of postoperative tumour recurrence and mortality in patients with hepatocellular carcinoma (HCC), but the underlying mechanism remains unclear. Accumulating evidence has demonstrated that programmed cell death 10 (PDCD10) plays an important role in many biological processes. However, the role of PDCD10 in HCC progression is still elusive. In this study, we aimed to explore the clinical significance and molecular function of PDCD10 in HCC. PDCD10 is significantly upregulated in HCC, which also correlates with aggressive clinicopathological characteristics and predicts poor prognosis of HCC patients after liver resection. High PDCD10 expression promotes HCC cell proliferation, migration, and invasion in vitro and tumour growth, metastasis in vivo. In addition, PDCD10 could facilitate epithelial-to-mesenchymal transition (EMT) of HCC cells. In terms of the mechanism, PDCD10 directly binds to the catalytic subunit of protein phosphatase 2A (PP2Ac) and increases its enzymatic activity, leading to the interaction of YAP and dephosphorylation of the YAP protein. This interaction contributes to YAP nuclear translocation and transcriptional activation. PP2Ac is necessary for PDCD10-mediated HCC progression. Knocking down PP2Ac abolished the tumour-promoting role of PDCD10 in the migration, invasion and EMT of HCC. Moreover, a PP2Ac inhibitor (LB100) could restrict tumour growth and metastasis of HCC with high PDCD10 expression. Collectively, PDCD10 promotes EMT and the progression of HCC by interacting with PP2Ac to promote YAP activation, which provides new insight into the mechanism of cancer metastasis. PDCD10 may be a potential prognostic biomarker and therapeutic target for HCC.


Author(s):  
Chang Liu ◽  
Zecheng Jiang ◽  
Zhongjie Pan ◽  
Liang Yang

Atherosclerosis is a chronic progressive inflammatory vascular disease, which is an important pathological basis for inducing a variety of cardio-cerebrovascular diseases. As a kind of inflammatory cells, macrophages are the most abundant immune cells in atherosclerotic plaques and participate in the whole process of atherosclerosis and are the most abundant immune cells in atherosclerotic plaques. Recent studies have shown that programmed cell death plays a critical role in the progression of many diseases. At present, it is generally believed that the programmed death of macrophages can affect the development and stability of atherosclerotic vulnerable plaques, and the intervention of macrophage death may become the target of atherosclerotic therapy. This article reviews the role of macrophage programmed cell death in the progression of atherosclerosis and the latest therapeutic strategies targeting macrophage death within plaques.


Oncotarget ◽  
2017 ◽  
Vol 8 (16) ◽  
pp. 26789-26801 ◽  
Author(s):  
Nora Ness ◽  
Sigve Andersen ◽  
Mehrdad Rakaee Khanehkenari ◽  
Cecilie V. Nordbakken ◽  
Andrej Valkov ◽  
...  

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