Sphingosine 1-Phosphate Receptor 2 Induces Otoprotective Responses to Cisplatin Treatment

Wang, Wei; Shanmugam, Muthu K.; Xiang, Peng; Yam, Ting Yu Amelia; Kumar, Vineet; Chew, Wee; Chang, Jing; Ali, Muhammad Zulfaqar; Reolo, Marie Jennifer; Peh, Yee Xin; Karim, Siti Nasuha Binte Abdul; Tan, Andrew Y. Y.; Sanda, Takaomi; Sethi, Gautam; Herr, Deron R.

doi:10.3390/cancers12010211

Cited by 24 publications

(15 citation statements)

References 68 publications

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“…However, despite its great potential in the treatment of cancer, the use of CP in cancer therapy has a number of disadvantages [55]. One of these is adverse effects on the body's organs and systems resulting from increased production of ROS and stimulation of mitochondrial dysfunction [56][57][58][59].…”

Section: Cisplatin In Cancer Therapymentioning

confidence: 99%

Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance

Ashrafizadeh

Zarrabi

Hushmandi

et al. 2020

IJMS

Self Cite

196

103

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Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial–mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell–cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-κB (NF-ĸB), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure.

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Section: Cisplatin In Cancer Therapymentioning

confidence: 99%

Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance

Ashrafizadeh

Zarrabi

Hushmandi

et al. 2020

IJMS

Self Cite

196

103

View full text Add to dashboard Cite

show abstract

“…Cisplatin (CP) is a platinumcontaining drug that was first discovered in 1965 and became famous due to its great antimicrobial activity. More experiments demonstrated that platinum-containing agents can possess anti-cancer activity [8][9][10][11][12][13]. As an electrophilic reagent, platinum can interact with nucleophilic residues of nucleobases, including guanine and adenosine by forming covalent bonds.…”

Section: Introductionmentioning

confidence: 99%

Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies

et al. 2021

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The failure of chemotherapy is a major challenge nowadays, and in order to ensure effective treatment of cancer patients, it is of great importance to reveal the molecular pathways and mechanisms involved in chemoresistance. Cisplatin (CP) is a platinum-containing drug with anti-tumor activity against different cancers in both pre-clinical and clinical studies. However, drug resistance has restricted its potential in the treatment of cancer patients. CP can promote levels of free radicals, particularly reactive oxygen species (ROS) to induce cell death. Due to the double-edged sword role of ROS in cancer as a pro-survival or pro-death mechanism, ROS can result in CP resistance. In the present review, association of ROS with CP sensitivity/resistance is discussed, and in particular, how molecular pathways, both upstream and downstream targets, can affect the response of cancer cells to CP chemotherapy. Furthermore, anti-tumor compounds, such as curcumin, emodin, chloroquine that regulate ROS and related molecular pathways in increasing CP sensitivity are described. Nanoparticles can provide co-delivery of CP with anti-tumor agents and by mediating photodynamic therapy, and induce ROS overgeneration to trigger CP sensitivity. Genetic tools, such as small interfering RNA (siRNA) can down-regulate molecular pathways such as HIF-1α and Nrf2 to promote ROS levels, leading to CP sensitivity. Considering the relationship between ROS and CP chemotherapy, and translating these findings to clinic can pave the way for effective treatment of cancer patients.

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“…In order to promote antitumor activity of chemotherapeutic agents, high doses of these agents are applied that substantially enhances side effects on other organs of body. Ototoxicity [ 9 ], hepatotoxicity [ 10 ], nephrotoxicity [ 11 ] and cardiotoxicity [ 12 ] are a few of adverse effects of chemotherapeutic agents.…”

Section: Introductionmentioning

confidence: 99%

Polychemotherapy with Curcumin and Doxorubicin via Biological Nanoplatforms: Enhancing Antitumor Activity

et al. 2020

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Doxorubicin (DOX) is a well-known chemotherapeutic agent extensively applied in the field of cancer therapy. However, similar to other chemotherapeutic agents such as cisplatin, paclitaxel, docetaxel, etoposide and oxaliplatin, cancer cells are able to obtain chemoresistance that limits DOX efficacy. In respect to dose-dependent side effect of DOX, enhancing its dosage is not recommended for effective cancer chemotherapy. Therefore, different strategies have been considered for reversing DOX resistance and diminishing its side effects. Phytochemical are potential candidates in this case due to their great pharmacological activities. Curcumin is a potential antitumor phytochemical isolated from Curcuma longa with capacity of suppressing cancer metastasis and proliferation and affecting molecular pathways. Experiments have demonstrated the potential of curcumin for inhibiting chemoresistance by downregulating oncogene pathways such as MMP-2, TGF-β, EMT, PI3K/Akt, NF-κB and AP-1. Furthermore, coadministration of curcumin and DOX potentiates apoptosis induction in cancer cells. In light of this, nanoplatforms have been employed for codelivery of curcumin and DOX. This results in promoting the bioavailability and internalization of the aforementioned active compounds in cancer cells and, consequently, enhancing their antitumor activity. Noteworthy, curcumin has been applied for reducing adverse effects of DOX on normal cells and tissues via reducing inflammation, oxidative stress and apoptosis. The current review highlights the anticancer mechanism, side effects and codelivery of curcumin and DOX via nanovehicles.

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Sphingosine 1-Phosphate Receptor 2 Induces Otoprotective Responses to Cisplatin Treatment

Cited by 24 publications

References 68 publications

Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance

Association of the Epithelial–Mesenchymal Transition (EMT) with Cisplatin Resistance

Elucidating Role of Reactive Oxygen Species (ROS) in Cisplatin Chemotherapy: A Focus on Molecular Pathways and Possible Therapeutic Strategies

Polychemotherapy with Curcumin and Doxorubicin via Biological Nanoplatforms: Enhancing Antitumor Activity

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