Current Opinions on Chemoresistance: An Overview

Hasan, Sadid A.; Taha, Ruba; Omri, Halima El

doi:10.6026/97320630014080

Cited by 46 publications

(32 citation statements)

References 37 publications

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“…Emerging evidences have linked miR-155 with migration and metastasis in multiple cancers [25,31], however its relevance in oral cancer with drug resistance is not clear. We therefore next intended to evaluate the effect of miR-155 on the migration of cis Res cells by scratch assay.…”

Section: Mir-155 Upregulation Mediates Epithelial To Mesenchymal Tranmentioning

confidence: 99%

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

et al. 2020

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Cisplatin is used as chemotherapeutic drug for oral squamous cell carcinoma (OSCC). However, OSCC cells develop resistance following long-term cisplatin exposure. Resistance against cisplatin chemo-therapy is accredited to the process of epithelial-to-mesenchymal transition, which in-turn has been linked to tumorrecurrence. miRNA deregulation, a common event in cancer, plays contributory role in chemo-resistance. Exosomes acts as the natural cargo for miRNA and facilitates inter-cell communication in the tumor micro-environment. Hence, exosomal-mediated miRNA transference may play essential role in drug resistance and serve as a target for cancer-therapy. miR-155 upregulation in OSCC has been described, however, its relevance in the observed chemo-resistance is unclear and also, if exosomes have any role in miR-155 regulation remain elusive. In the present study, we document for the first time the critical role of exosomes in mediating increments in miR-155 expression in OSCC cells that have acquired cisplatin resistance (cis Res cells). Importantly, exosomal transfer from cis Res to the cisplatin sensitive (cis Sens) cells was found to confer significant miR-155 induction in the recipient cis Sens cells. Restoration of miR-155 expression in cis Sens cells following miR-155 mimics treatment led to epithelial to mesenchymal transition, enhancements in their migratory potential as well as acquisition of resistant phenotype. Notably, similar augmentations in the migratory and chemo-resistant traits were seen upon delivery of exosomes from cis Res to the recipient cis Sens cells. Overall, our findings establish the significance of exosomalmediated miR-155 shuttling in the cisplatin-chemoresistance, commonly observed in OSCC cells, thereby providing rationale for targeting miR-155 signalling for oral cancer therapy.

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Section: Mir-155 Upregulation Mediates Epithelial To Mesenchymal Tranmentioning

confidence: 99%

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

et al. 2020

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“…Chemoresistance, a feature by which the cancer cells become less sensitive to chemotherapeutic drugs forms one of the major reason for this disease relapse and pose a major challenge in cancer treatment regime ( 5 ). The factors contributing to chemoresistance are many, with cancer stemness, impaired drug transport as well as targeted gene mutations being the most highlighted ones ( 6 ). Though mutations in several genes has been extensively correlated to CRC development, TP53 (p53) forms one of the most commonly mutated genes in cancer ( 7 ).…”

Section: Introductionmentioning

confidence: 99%

Dysregulated Phosphorylation of p53, Autophagy and Stemness Attributes the Mutant p53 Harboring Colon Cancer Cells Impaired Sensitivity to Oxaliplatin

et al. 2020

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Colorectal cancer (CRC) forms one of the highest ranked cancer types in the world with its increasing incidence and mortality rates despite the advancement in cancer therapeutics. About 50% of human CRCs are reported to have defective p53 expression resultant of TP53 gene mutation often contributing to drug resistance. The current study was aimed to investigate the response of wild-type TP53 harboring HCT 116 and mutant TP53 harboring HT 29 colon cancer cells to chemotherapeutic drug oxaliplatin (OX) and to elucidate the underlying molecular mechanisms of sensitivity/resistance in correlation to their p53 status. OX inhibited growth of wild-type p53-harboring colon cancer cells via p53/p21-Bax mediated apoptosis. Our study revealed that dysregulated phosphorylation of p53, autophagy as well as cancer stemness attributes the mutant p53-harboring colon cancer cells impaired sensitivity to OX.

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“…Cancer MDR refers to the phenomenon that tumor cells are resistant to the effects of numerous antineoplastic drugs, regardless of their chemical structure or target. MDR in tumors is a complex process and involves numerous mechanisms ( 25 ).…”

Section: Discussionmentioning

confidence: 99%

Salvianolic acid B reverses multidrug resistance in nude mice bearing human colon cancer stem cells

et al. 2018

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Salvianolic acid B (SalB) is a water-soluble phenolic compound, extractable from Salvia miltiorrhiza, and has previously been demonstrated to reverse tumor multidrug resistance (MDR) in colon cancer cells. Cancer stem cells (CSCs) are closely associated with drug resistance. Therefore, establishing a nude mouse model bearing human colon CSCs is important for the study of the mechanisms underlying colon cancer drug resistance as well as the reversal of drug resistance. The present study aimed to establish a nude mouse model bearing human colon CSCs and to investigate the effects of SalB on the drug resistance exhibited by the nude mouse model as well as determine its underlying mechanism. Cells from two colon cancer cell lines (LoVo and HCT-116) were cultured in serum-free medium to obtain CSCs-enriched spheroid cells. Following this, nude mice were transplanted with LoVo and HCT-116 colon CSCs to establish the CSC nude mouse model, which was subsequently demonstrated to exhibit MDR. The results of the present study revealed that following treatment with SalB, the chemotherapeutic drug resistance of xenografts was reversed to a certain extent. Western blot analysis was performed to investigate the expression levels of cluster of differentiation (CD)44, CD133, transcription factor sox-2 (SOX2) and ATP-binding cassette sub-family G member 2 (ABCG2) proteins, and the results demonstrated that treatment with SalB downregulated the expression of CD44, SOX2 and ABCG2 proteins in both LoVo and HCT-116 colon CSCs xenografts. In conclusion, the results of the present study revealed that a serum-free suspension method can be performed to successfully isolate colon CSCs. In addition, a nude mice bearing colon CSCs animal model was successfully established, and associated tumors were confirmed to exhibit MDR. Furthermore, SalB was demonstrated to successfully reverse MDR in nude mice bearing LoVo and HCT-116 colon CSCs, as well as suppress the expression of CD44, SOX2 and ABCG2 proteins.

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Current Opinions on Chemoresistance: An Overview

Cited by 46 publications

References 37 publications

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

Dysregulated Phosphorylation of p53, Autophagy and Stemness Attributes the Mutant p53 Harboring Colon Cancer Cells Impaired Sensitivity to Oxaliplatin

Salvianolic acid B reverses multidrug resistance in nude mice bearing human colon cancer stem cells

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