Establishment and characterization of a cisplatin-resistant cell line, KB-R, derived from oral carcinoma cell line, KB

Negoro, Kohei; Yamano, Y.; Fushimi, Kazuaki; Saito, Kengo; Nakatani, Ken; Shiiba, Masashi; Yokoe, Hidetaka; Bukawa, Hiroki; Uzawa, Katsuhiro; Wada, Takuro; Tanzawa, Hideki; Fujita, Shigeyuki

doi:10.3892/ijo.30.6.1325

Cited by 20 publications

(20 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This probably results from the method used to select ciprofloxacin-resistant cells (i.e., long-term culture at progressively increasing ciprofloxacin concentrations), which is prone to select for multiple mechanisms of resistance (11). Several examples indeed document the concomitant overexpression of different efflux transporters in drug-resistant cell lines (P-glycoprotein and MRP1 in doxorubicin-or vincristine-resistant cells [5,8], MRP1 and MRP2 in cisplatin-resistant cells [27], and P-glycoprotein and MRP2 in colchicine-resistant cells [3]). Yet this overexpression of Mrp2 is most likely unrelated to ciprofloxacin efflux, as it remains slightly elevated in revertant cells (versus wild-type cells) when ciprofloxacin accumulation and Mrp4 expression have both returned to control values.…”

Section: Discussionmentioning

confidence: 99%

Identification of the Efflux Transporter of the Fluoroquinolone Antibiotic Ciprofloxacin in Murine Macrophages: Studies with Ciprofloxacin-Resistant Cells

Márquez

Caceres

Mingeot‐Leclercq

et al. 2009

Antimicrob Agents Chemother

View full text Add to dashboard Cite

Ciprofloxacin, the most widely used totally synthetic antibiotic, is subject to active efflux mediated by a MRP-like transporter in wild-type murine J774 macrophages. To identify the transporter among the seven potential Mrps, we used cells made resistant to ciprofloxacin obtained by long-term exposure to increasing drug concentrations (these cells show less ciprofloxacin accumulation and provide a protected niche for ciprofloxacin-sensitive intracellular Listeria monocytogenes). In the present paper, we first show that ciprofloxacin-resistant cells display a faster efflux of ciprofloxacin which is inhibited by gemfibrozil (an unspecific MRP inhibitor). Elacridar, at a concentration known to inhibit P-glycoprotein and breast cancer resistance protein (

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of the Efflux Transporter of the Fluoroquinolone Antibiotic Ciprofloxacin in Murine Macrophages: Studies with Ciprofloxacin-Resistant Cells

Márquez

Caceres

Mingeot‐Leclercq

et al. 2009

Antimicrob Agents Chemother

View full text Add to dashboard Cite

show abstract

“…Zhe Zhu 1,2& , Cun-Ping Wang 2& , Yin-Feng Zhang 3 , Lin Nie 1 * rate of initial responses, cisplatin resistance limits its utilizations in cancer patients because some cancer cells develop acquired cisplatin resistance eventually (Negoro et al, 2007;Galluzzi et al, 2012;Barr et al, 2013). The mechanisms of cisplatin resistance are not fully understood yet.…”

Section: Microrna-100 Resensitizes Resistant Chondrosarcoma Cells To mentioning

confidence: 99%

MicroRNA-100 Resensitizes Resistant Chondrosarcoma Cells to Cisplatin through Direct Targeting of mTOR

Zhu

Wang²,

Zhang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

View full text Add to dashboard Cite

Chondrosarcomas are malignant cartilage-forming tumors of bone which exhibit resistance to both chemotherapy and radiation treatment. miRNAs have been well demonstrated to regulate gene expression and play essential roles in a variety of biological processes, including proliferation, differentiation, migration, cell cycling and apoptosis. In this study, we obtained evidence that miR-100 acts as a tumor suppressor in human chondrosarcomas. Interestingly, cisplatin resistant chondrosarcoma cells exhibit decreased expression of miR-100 compared with parental cells. In addition, we identified mTOR as a direct target of miR-100. Overexpression of miR-100 complementary pairs to the 3' untranslated region (UTR) of mTOR, resulted in sensitization of cisplatin resistant cells to cisplatin. Moreover, recovery of the mTOR pathway by overexpression of S6K desensitized the chondrosarcoma cells to cisplatin, suggesting the miR-100-mediated sensitization to cisplatin dependent on inhibition of mTOR. In summary, the present studies highlight miR-100 as a tumor suppressor in chondrosarcoma contributing to anti-chemoresistance. Overexpression of miR-100 might be exploited as a therapeutic strategy along with cisplatin-based combined chemotherapy for the treatment of clinical chondrosarcoma patients.

show abstract

“…In the past few decades, IMR90 have been used extensively as model fibroblasts for a wide variety of research purposes [27]. The KB cell line used in this study was not resistant to cisplatin, although research efforts have been made to establish a cisplatin-resistant KB cell line [28]. Few scientific reports are available discussing the combination of these three tested drugs for oral cancer treatment.…”

Section: Discussionmentioning

confidence: 97%

Optimized combinations of bortezomib, camptothecin, and doxorubicin show increased efficacy and reduced toxicity in treating oral cancer

Matsuo

Lin

et al. 2015

Anti-Cancer Drugs

View full text Add to dashboard Cite

Oral cancer continues to be a major cause of morbidity and mortality worldwide. Treatment of oral cancer with combinatorial drugs is increasingly being performed as drugs with different molecular targets often exert synergistic effects, thereby enhancing treatment efficacy. Current combinatorial drug regimens often combine the tolerable dosages of individual drugs. However, the optimized ratio of a drug combination and sequence of drug administration could contribute toward the synergy, leading to increased efficacy and reduced dosages. This report aims to study the possible synergistic effects of three anticancer drugs, a proteasome inhibitor, bortezomib, a topoisomerase I inhibitor, Camptothecin, and a DNA intercalation drug, Doxorubicin, when used in combination for treating oral cancer. To rapidly optimize the three-drug regimen with minimal experimental efforts, a Feedback System Control optimization technique, a recent platform technique developed particularly for drug combination screening, was applied. The optimized regimen showed a therapeutic window (death rate difference between cancer cells and normal cells) close to 100%. This is the first report on the use of a combination of bortezomib, Camptothecin, and Doxorubicin in the treatment of oral cancer. Our results indicate that to have the most synergistic anticancer effect, the drugs in the optimized regimen should be dosage specific and ratio specific. Furthermore, the sequence of drug administration plays a vital role in ensuring that the combination is effective. The optimized regimen reported here has the potential to considerably increase the cure rate of oral cancer and reduce the toxicity of chemotherapy.

show abstract

Establishment and characterization of a cisplatin-resistant cell line, KB-R, derived from oral carcinoma cell line, KB

Cited by 20 publications

References 19 publications

Identification of the Efflux Transporter of the Fluoroquinolone Antibiotic Ciprofloxacin in Murine Macrophages: Studies with Ciprofloxacin-Resistant Cells

Identification of the Efflux Transporter of the Fluoroquinolone Antibiotic Ciprofloxacin in Murine Macrophages: Studies with Ciprofloxacin-Resistant Cells

MicroRNA-100 Resensitizes Resistant Chondrosarcoma Cells to Cisplatin through Direct Targeting of mTOR

Optimized combinations of bortezomib, camptothecin, and doxorubicin show increased efficacy and reduced toxicity in treating oral cancer

Contact Info

Product

Resources

About