The Role of Ferroptosis Regulators in the Prognosis, Immune Microenvironment and Gemcitabine Resistance of Pancreatic Cancer

2020 ◽  
Author(s):  
Rong Tang ◽  
Jie Hua ◽  
Jin Xu ◽  
Chen Liang ◽  
Qingcai Meng ◽  
...  
Oncogene ◽  
2018 ◽  
Vol 38 (10) ◽  
pp. 1764-1777 ◽  
Author(s):  
Yanfei Jia ◽  
Dongsheng Gu ◽  
Jun Wan ◽  
Beiqin Yu ◽  
Xiaoli Zhang ◽  
...  

Cancers ◽  
2017 ◽  
Vol 9 (12) ◽  
pp. 142 ◽  
Author(s):  
Omar Elaskalani ◽  
Marco Falasca ◽  
Niamh Moran ◽  
Michael Berndt ◽  
Pat Metharom

2020 ◽  
Vol 8 (21) ◽  
pp. 1347-1347
Author(s):  
Rong Tang ◽  
Jie Hua ◽  
Jin Xu ◽  
Chen Liang ◽  
Qingcai Meng ◽  
...  

2017 ◽  
Vol 8 (7) ◽  
pp. e2924-e2924 ◽  
Author(s):  
Yuran Gao ◽  
Zhicheng Zhang ◽  
Kai Li ◽  
Liying Gong ◽  
Qingzhu Yang ◽  
...  

AbstractThe acquisition of epithelial–mesenchymal transition (EMT) and/or existence of a sub-population of cancer stem-like cells (CSC) are associated with malignant behavior and chemoresistance. To identify which factor could promote EMT and CSC formation and uncover the mechanistic role of such factor is important for novel and targeted therapies. In the present study, we found that the long intergenic non-coding RNA linc-DYNC2H1-4 was upregulated in pancreatic cancer cell line BxPC-3-Gem with acquired gemcitabine resistance. Knockdown of linc-DYNC2H1-4 decreased the invasive behavior of BxPC-3-Gem cells while ectopic expression of linc-DYNC2H1-4 promoted the acquisition of EMT and stemness of the parental sensitive cells. Linc-DYNC2H1-4 upregulated ZEB1, the EMT key player, which led to upregulation and downregulation of its targets vimentin and E-cadherin respectively, as well as enhanced the expressions of CSC makers Lin28, Nanog, Sox2 and Oct4. Linc-DYNC2H1-4 is mainly located in the cytosol. Mechanically, it could sponge miR-145 that targetsZEB1,Lin28,Nanog,Sox2,Oct4to restore these EMT and CSC-associated genes expressions. We proved thatMMP3, the nearby gene of linc-DYNC2H1-4 in the sense strand, was also a target of miR-145. Downregulation ofMMP3by miR-145 was reverted by linc-DYNC2H1-4, indicating that competing with miR-145 is one of the mechanisms for linc-DYNC2H1-4 to regulateMMP3. In summary, our results explore the important role of linc-DYNC2H1-4 in the acquisition of EMT and CSC, and the impact it has on gemcitabine resistance in pancreatic cancer cells.


Pancreatology ◽  
2019 ◽  
Vol 19 ◽  
pp. S77
Author(s):  
Zhefang Wang ◽  
Qin Jie ◽  
Jiangang Zhao ◽  
Jiahui Li ◽  
Marie Popp ◽  
...  

Pancreatology ◽  
2015 ◽  
Vol 15 (3) ◽  
pp. S27-S28
Author(s):  
Felix Lämmerhirt ◽  
Markus M. Lerch ◽  
Frank Ulrich Weiss

2019 ◽  
Author(s):  
Sanchita Rauth ◽  
Saswati Karmakar ◽  
Ashu Shah ◽  
Rama Krishna Nimmakayala ◽  
Rakesh Bhatia ◽  
...  

2021 ◽  
Vol 22 (18) ◽  
pp. 9914
Author(s):  
Giovanni Brandi ◽  
Silvia Turroni ◽  
Florencia McAllister ◽  
Giorgio Frega

Recent pieces of evidence have emerged on the relevance of microorganisms in modulating responses to anticancer treatments and reshaping the tumor-immune microenvironment. On the one hand, many studies have addressed the role of the gut microbiota, providing interesting correlative findings with respect to etiopathogenesis and treatment responses. On the other hand, intra-tumoral bacteria are being recognized as intrinsic and essential components of the cancer microenvironment, able to promote a plethora of tumor-related aspects from cancer growth to resistance to chemotherapy. These elements will be probably more and more valuable in the coming years in early diagnosis and risk stratification. Furthermore, microbial-targeted intervention strategies may be used as adjuvants to current therapies to improve therapeutic responses and overall survival. This review focuses on new insights and therapeutic approaches that are dawning against pancreatic cancer: a neoplasm that arises in a central metabolic “hub” interfaced between the gut and the host.


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