scholarly journals Oncogenic Mutant p53 Gain of Function Nourishes the Vicious Cycle of Tumor Development and Cancer Stem-Cell Formation

2016 ◽  
Vol 6 (10) ◽  
pp. a026203 ◽  
Author(s):  
Yoav Shetzer ◽  
Alina Molchadsky ◽  
Varda Rotter
Keyword(s):  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cell Formation ◽  
Tumor Development ◽  
Mutant P53 ◽  
Vicious Cycle ◽  
Gain Of Function

scholarly journals The cancer stem cell paradigm: a new understanding of tumor development and treatment

2010 ◽  
Vol 14 (6) ◽  
pp. 621-632 ◽  
Author(s):  
Johnathan D Ebben ◽  
Daniel M Treisman ◽  
Michael Zorniak ◽  
Raman G Kutty ◽  
Paul A Clark ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cancer Stem Cell ◽  
Tumor Development

A possible interplay between HR‐HPV and stemness in tumor development: an in vivo investigation of CD133 as a putative marker of cancer stem cell in HPV18‐infected KB cell line

Apmis ◽  
2020 ◽  
Vol 128 (12) ◽  
pp. 637-646
Author(s):  
Salvatore Maria ◽  
Angela Santoro ◽  
Maria Pia Fuggetta ◽  
Romina Rocchetti ◽  
Andrea Cottarelli ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cancer Stem Cell ◽  
Cell Line ◽  
Tumor Development ◽  
Putative Marker

scholarly journals EBV LMP1-activated mTORC1 and mTORC2 Coordinately Promote Nasopharyngeal Cancer Stem Cell Properties

2021 ◽  
Author(s):  
Nannan Zhu ◽  
Qian Wang ◽  
Zhidong Wu ◽  
Yan Wang ◽  
Mu-Sheng Zeng ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cancer Stem Cell ◽  
Side Population ◽  
Nasopharyngeal Cancer ◽  
Chemotherapy Resistance ◽  
Cell Formation ◽  
Migration And Invasion ◽  
Tumor Initiation ◽  
Mesenchymal Transition ◽  
Mtorc1 Signaling

Epstein-Barr Virus (EBV) is associated with several malignant diseases, including Burkitt’s lymphoma, nasopharyngeal carcinoma (NPC), certain types oflymphomas,and a portion of gastric cancers. Virus-encoded oncoprotein LMP1 induces the epithelial-to-mesenchymal transition (EMT), leading to cancer stem cell formation. In the current study, we investigated how LMP1 contributes to cancer stem cell development in NPC. We found that LMP1 plays an essential role in acquiring CSC characteristics, including tumor initiation, metastasis, and therapeutic resistance by activating the PI3K/mTOR/Akt signaling pathway. We dissected the functions of distinct signaling (mTORC1 and mTORC2) in the acquisition of different CSC characteristics. Side population (SP) formation, which represents the chemotherapy resistance feature of CSC, requires mTORC1 signaling. Tumor initiation capability is mainly attributed to mTORC2, which confers on NPC the capabilities of proliferation and survival by activating mTORC2 downstream genes c-Myc. Both mTORC1 and mTORC2 enhance cell migration and invasion of NPC cells, suggesting that mTORC1/2 co-regulate metastasis of NPC. The revelation of the roles of the mTOR signaling pathways in distinct tumorigenic features provides a guideline for designing efficient therapies by choosing specific mTOR inhibitors targeting mTORC1, mTORC2, or both to achieve durable remission of NPC in patients.

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