Cancer stem cells and the impact of Chinese herbs, isolates and other complementary medical botanicals: a review

2012 ◽  
Vol 10 (5) ◽  
pp. 493-503 ◽  
Author(s):  
DA Weber
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Chinese Herbs ◽  
The Impact

The impact of fusion genes on cancer stem cells and drug resistance

2021 ◽  
Author(s):  
Saurav Panicker ◽  
Sivaramakrishnan Venkatabalasubramanian ◽  
Surajit Pathak ◽  
Satish Ramalingam
Keyword(s):  
Stem Cells ◽  
Drug Resistance ◽  
Cancer Stem Cells ◽  
Fusion Genes ◽  
The Impact

scholarly journals MicroRNA-28-5p Regulates Liver Cancer Stem Cell Expansion via IGF-1 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Qing Xia ◽  
Tao Han ◽  
Pinghua Yang ◽  
Ruoyu Wang ◽  
Hengyu Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Liver Cancer ◽  
Critical Role ◽  
Self Renewal ◽  
Sorafenib Treatment ◽  
The Impact

Background. MicroRNAs (miRNAs) play a critical role in the regulation of cancer stem cells (CSCs). However, the role of miRNAs in liver CSCs has not been fully elucidated. Methods. Real-time PCR was used to detect the expression of miR-miR-28-5p in liver cancer stem cells (CSCs). The impact of miR-28-5p on liver CSC expansion was investigated both in vivo and in vitro. The correlation between miR-28-5p expression and sorafenib benefits in HCC was further evaluated in patient-derived xenografts (PDXs). Results. Our data showed that miR-28-5p was downregulated in sorted EpCAM- and CD24-positive liver CSCs. Biofunctional investigations revealed that knockdown miR-28-5p promoted liver CSC self-renewal and tumorigenesis. Consistently, miR-28-5p overexpression inhibited liver CSC’s self-renewal and tumorigenesis. Mechanistically, we found that insulin-like growth factor-1 (IGF-1) was a direct target of miR-28-5p in liver CSCs, and the effects of miR-28-5p on liver CSC’s self-renewal and tumorigenesis were dependent on IGF-1. The correlation between miR-28-5p and IGF-1 was confirmed in human HCC tissues. Furthermore, the miR-28-5p knockdown HCC cells were more sensitive to sorafenib treatment. Analysis of patient-derived xenografts (PDXs) further demonstrated that the miR-28-5p may predict sorafenib benefits in HCC patients. Conclusion. Our findings revealed the crucial role of the miR-28-5p in liver CSC expansion and sorafenib response, rendering miR-28-5p an optimal therapeutic target for HCC.

The Impact of Hypoxia and Mesenchymal Transition on Glioblastoma Pathogenesis and Cancer Stem Cells Regulation

2016 ◽  
Vol 88 ◽  
pp. 222-236 ◽  
Author(s):  
Michael Karsy ◽  
Jian Guan ◽  
Randy Jensen ◽  
L. Eric Huang ◽  
Howard Colman
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Mesenchymal Transition ◽  
The Impact

Impacts of microRNA-215 on cell proliferation and chemotherapy resistance in colon cancer and osteosarcoma

2009 ◽  
Vol 27 (15_suppl) ◽  
pp. 2542-2542
Author(s):  
J. Ju ◽  
B. Song ◽  
Y. Wang
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Stem Cells ◽  
Cell Lines ◽  
Chemotherapy Resistance ◽  
Osteosarcoma Cell ◽  
Colon Cancer Stem Cells ◽  
The Impact

2542 Background: Translational control plays a key role in resistance to anti-cancer drug treatment. MicroRNAs regulate gene expression at the post-transcriptional level, mainly by interacting with 3'-UTR of their mRNA targets. Methods: miR-215 was ectopically expressed by transient transfection in both human colon cancer cell lines and osteosarcoma cell lines. The impact of miR-215 on cell proliferation, cell cycle control, chemosensitivity and down stream targets were characterized. The expression of miR-215 in colorectal cancer specimens and normal adjacent tissues was quantified by real time-qRT-PCR analysis. Results: In this study, we discovered that miR-215 down-regulates the expression of both dihydrofolate reductase (DHFR) and thymidylate synthase (TS), two of the most important chemotherapeutic targets, in human osteosarcoma U-2 OS and colon cancer HCT-116 (wt-p53) cell lines. Cells with elevated miR-215 expression are more resistant to DHFR inhibitor methotrexate (MTX) or TS inhibitor Tomudex (TDX) treatment. Ectopically over-expressing miR-215 triggers reduced cell proliferation and increased G2 arrest, at least in part, through the induction of p53 and p21. miR-215 transfected cells with reduced proliferating phenotype were resist to MTX or TDX treatment due to deceased cell cycle in S phase. The expression of endogeneous miR-215 was highly elevated in CD133+/HI CD44+/HI colon cancer stem cells compared to CD133- CD44- colon cancer cells, suggesting that tumor stem cells may be avoiding cellular and DNA damage caused by chemotherapy with a reduced proliferating phenotype mediated by certain miRNAs such as miR-215. The elevated expression of miR-215 in colon cancer stem cells with slow proliferation rate and resistance to chemotherapy further supports the role of miR-215 in cell proliferation and chemotherapy resistance. Conclusions: miR-215 may have a unique potential as a novel therapeutic target and biomarker candidate in cancer. No significant financial relationships to disclose.

Do pancreas cancer stem cells play crucial role in survival outcome?

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e15721-e15721
Author(s):  
Gokce Askan ◽  
Ibrahim Halil Sahin ◽  
Marinela Capanu ◽  
Mesruh Turkekul ◽  
Kenneth H. Yu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cancer Stem Cells ◽  
Lung Metastasis ◽  
Specific Antigen ◽  
Survival Outcome ◽  
Significant Difference ◽  
Group 2 ◽  
The Impact ◽  
Group 1

e15721 Background: Recent studies indicate that pancreatic cancer stem cells (CSC) may predict disease behavior and survival outcomes of pancreatic ductal adenocarcinomas (PDACs) patients (pts). Several CSC markers have been reported in PDAC (Fitzgerald, TL, 2014). We herein evaluated the impact of CSC markers including CD44 and Epithelial Specific Antigen (ESA) on survival outcome of PDAC pts who had liver or lung metastasis after initial surgical resection (IR). Methods: Clinicopathologic features and survival of 59 PDACs were analyzed. Pts with IRB approval, and whom had available primary tumor tissue, were included. All neoplasms were immuno labeled with CD44 and ESA. Staining intensity was scored as weak (1), moderate (2), strong (3), while the staining pattern was scored as: few (1), patchy (2), and diffuse (3). The expression for CD44 and ESA was accepted positive if total score ≥4. Time from relapse to death (TRD) was estimated using the Kaplan-Meier method censoring patients that were alive at the last follow up. Survival curves were compared using the log-rank test Results: Of 59 pts, 42 (71 %) had liver, 10 (17%) had lung and 7 (12%) had both liver and lung metastasis. M/F = 34/25; mean age = 64.2 (range, 34-90). Patients were subcategorized as follows; thirteen cases were CD44 (+)/ESA (-) (group1) and 13 were CD44 (-)/ESA (+) (group 2). Eight (61.5%) of group 1 tumors and 2 (15.3%) of group 2 were poorly differentiated. At last follow-up, except one with 63 months survival, all pts died of disease with 23.3 months (range, 3-67) median OS. No significant difference in TRD was observed between group 1 (6.9 months) and 2 (13.8 months) (p = 0.62). However, we observed group 1 tumors had worse OS (12 months) compared to group 2 (36 months). Conclusions:A worse outcome trend was observed for pts with CD44 (+)/ESA (-), albeit not statistically significant and likely limited by small numbers. Further studies are warranted to evaluate the robustness of this observation.

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