MAGE-A11 expression contributes to cisplatin resistance in head and neck cancer

2017 ◽  
Vol 22 (3) ◽  
pp. 1477-1486 ◽  
Author(s):  
Stefan Hartmann ◽  
Leonie Zwick ◽  
Mario J. J. Scheurer ◽  
Andreas R. Fuchs ◽  
Roman C. Brands ◽  
...  
Keyword(s):  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Cisplatin Resistance

scholarly journals CD44s Induces miR-629-3p Expression in Association with Cisplatin Resistance in Head and Neck Cancer Cells

Cancers ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 856
Author(s):  
Junichiro Chikuda ◽  
Kurataka Otsuka ◽  
Iwao Shimomura ◽  
Kagenori Ito ◽  
Hiroaki Miyazaki ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Target Genes ◽  
Cisplatin Resistance ◽  
Apoptotic Cell ◽  
Standard Form ◽  
Therapeutic Effects ◽  
Gene Expressions

Cisplatin (cis-diamminedichloroplatinum II [CDDP] ) is a well-known chemotherapeutic drug that has been used for the treatment of various types of human cancers, including head and neck cancer. Cisplatin exerts anticancer effects by causing DNA damage, replication defects, transcriptional inhibition, cell cycle arrest, and the induction of apoptosis. However, drug resistance is one of the most serious problems with cancer chemotherapy, and it causes expected therapeutic effects to not always be achieved. Here, we analyzed global microRNA (miRNA) expression in CD44 standard form (CD44s)-expressing SAS cells, and we identified miR-629-3p as being responsible for acquiring anticancer drug resistance in head and neck cancer. The introduction of miR-629-3p expression inhibited apoptotic cell death under cisplatin treatment conditions, and it promoted cell migration. Among the computationally predicted target genes of miR-629-3p, we found that a number of gene expressions were suppressed by the transfection with miR-629-3p. Using a xenografting model, we showed that miR-629-3p conferred cisplatin resistance to SAS cells. Clinically, increased miR-629-3p expression tended to be associated with decreased survival in head and neck cancer patients. In conclusion, our data suggest that the increased expression of miR-629-3p provides a mechanism of cisplatin resistance in head and neck cancer and may serve as a therapeutic target to reverse chemotherapy resistance.

Abstract 2563: Upregulation of miR-155 is associated with cisplatin resistance in the head and neck cancer UMSCC-10B/15S cells

2010 ◽  
Author(s):  
Ashim Gupta ◽  
Shoumin Zhu ◽  
Mohit Sachdeva ◽  
Krishna Rao ◽  
Thomas Robbins ◽  
...  
Keyword(s):  
Head And Neck Cancer ◽  
Head And Neck ◽  
Neck Cancer ◽  
Cisplatin Resistance

Decreased cisplatin/DNA adduct formation is associated with cisplatin resistance in human head and neck cancer cell lines

2000 ◽  
Vol 46 (4) ◽  
pp. 255-262 ◽  
Author(s):  
Zejia Yang ◽  
Patrick J. Faustino ◽  
Paul A. Andrews ◽  
Rachelle Monastra ◽  
Audrey A. Rasmussen ◽  
...  
Keyword(s):  
Head And Neck Cancer ◽  
Head And Neck ◽  
Cell Lines ◽  
Cancer Cell ◽  
Neck Cancer ◽  
Cisplatin Resistance ◽  
Human Head ◽  
Cancer Cell Lines ◽  
Adduct Formation ◽  
Dna Adduct

scholarly journals Selective Activation of Cancer Stem Cells by Size-Specific Hyaluronan in Head and Neck Cancer

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Marisa Shiina ◽  
Lilly Y. W. Bourguignon
Keyword(s):  
Head And Neck Cancer ◽  
Stem Cell ◽  
Head And Neck ◽  
Cancer Progression ◽  
Neck Cancer ◽  
Cisplatin Resistance ◽  
Human Head ◽  
Stem Cell Marker ◽  
Oncogenic Signaling ◽  
Selective Activation

We determined that human head and neck cancer cells (HSC-3 cell line) contain a subpopulation displaying cancer stem cell (CSC) properties and are very tumorigenic. Specifically, we investigated whether different sizes of hyaluronan (HA) (e.g., 5 kDa, 20 kDa, 200 kDa, or 700 kDa-HA-sizes) play a role in regulating these CSCs. First, we observed that 200 kDa-HA (but not other sizes of HA) preferentially induces certain stem cell marker expression resulting in self-renewal and clonal formation of these cells. Further analyses indicate that 200 kDa-HA selectively stimulates the expression of a panel of microRNAs (most noticeably miR-10b) in these CSCs. Survival protein (cIAP-1) expression was also stimulated by 200 kDa-HA in these CSCs leading to cisplatin resistance. Furthermore, our results indicate that the anti-miR-10 inhibitor not only decreases survival protein expression, but also increases chemosensitivity of the 200 kDa-HA-treated CSCs. These findings strongly support the contention that 200 kDa-HA plays a pivotal role in miR-10 production leading to survival protein upregulation and chemoresistance in CSCs. Together, our findings suggest that selective activation of oncogenic signaling by certain sizes of HA (e.g., 200 kDa-HA) may be instrumental in the formation of CSC functions leading to tumor cell survival and chemoresistance in head and neck cancer progression.

Sign in / Sign up

Export Citation Format

Share Document