Mebendazole And Cisplatin: A Hopeful Combination For Ovarian Cancer

This article discusses two studies identifying the potential use of mebendazole for chemotherapy-resistant ovarian cancer.

Introduction

Ovarian cancer is the third most common cancer among women and ranks as the second leading cause of gynecologic cancer-related deaths worldwide.

Often diagnosed at an advanced stage, ovarian cancer presents significant challenges in treatment and management.

The standard approach involves surgical resection followed by systemic chemotherapy, typically combining platinum-based drugs like cisplatin with paclitaxel.

While initial responses to chemotherapy are promising, many patients face a grim reality: recurrence and the development of resistance to chemotherapy.

Cisplatin resistance is particularly concerning because it limits treatment options, rendering standard therapies ineffective and leaving patients with fewer options.

This underscores the urgent need for innovative strategies to combat cisplatin resistance and improve outcomes for ovarian cancer patients.

One promising approach is repurposing existing drugs, such as the antiparasitic agent mebendazole (MBZ).

The Potential of Mebendazole in Ovarian Cancer Treatment

Two groundbreaking studies, published in Gynecologic Oncology (January 2021) and Aging (July 2021), highlight the potential of mebendazole, a common antiparasitic drug, as a powerful weapon against ovarian cancer. Here are the key findings:

1. Study from Gynecologic Oncology: Mebendazole as a Standalone Therapy

This study explored the effects of mebendazole on ovarian cancer using laboratory models and patient-derived samples, focusing on its ability to inhibit tumor growth and prevent cancer establishment.

• Key Results:
  • Mebendazole effectively inhibited the growth of ovarian cancer cells at very low (nanomolar) concentrations.
  • It also prevented tumor establishment in mice at 50 mg/kg.
  • Importantly, mebendazole’s mechanism of action was independent of p53, a gene frequently mutated in ovarian cancer. Instead, it induced the expression of p21 and disrupted microtubules within the cancer cells.
• Combination Therapy with PRIMA-1MET:
  • PRIMA-1MET, a compound designed to reactivate mutant p53, was shown to work synergistically with mebendazole to induce apoptosis (cell death) in cancer cells.
  • Combining the two drugs inhibited tumor growth more effectively than alone, providing a promising basis for future combination therapies.

2. Study from Aging: Overcoming Cisplatin Resistance

The second study specifically addressed the challenge of cisplatin-resistant ovarian cancer, a major hurdle in treatment.

Researchers investigated whether mebendazole could help overcome this resistance and improve the efficacy of cisplatin.

• Key Findings:
  • Mebendazole significantly inhibited the growth of both parental and cisplatin-resistant ovarian cancer cells at low micromolar concentrations.
  • Mebendazole (MBZ) significantly slowed cell growth, prevented cells from moving and repairing wounds, and caused cell death in both regular and drug-resistant cells, even at very low doses.
    • In ovarian cancer treatment, “wounds” refers to cellular damage or gaps in tissue or cell layers. These are not literal skin wounds but represent areas where cancer cells or normal cells need to migrate, grow, or repair gaps within the tumor microenvironment or surrounding tissues.
  • Combined with cisplatin, mebendazole synergistically suppressed tumor growth and induced apoptosis in cisplatin-resistant cancer cells.
• Mechanisms of Action:
  • Mebendazole blocked several cancer-associated signaling pathways, including ELK/SRF, NFKB, MYC/MAX, and E2F/DP1.
  • By disrupting these pathways, mebendazole sensitized cancer cells to cisplatin and inhibited their growth more effectively inhibited their growth.
• Animal Model Results:
  • In mouse models with cisplatin-resistant ovarian cancer, the combination of mebendazole and cisplatin significantly blunted tumor growth, showing the potential for clinical application.

Why Mebendazole?

Mebendazole is a well-known antiparasitic drug safely used for decades to treat conditions like pinworm infections. Its established safety profile, low cost, and oral availability make it an attractive candidate for repurposing in cancer treatment.

The studies highlighted above demonstrate that mebendazole has direct anti-cancer effects and enhances the effectiveness of existing chemotherapy drugs like cisplatin.

Implications for the Future

The findings from these studies open the door for further clinical trials to evaluate the safety and efficacy of mebendazole in ovarian cancer patients, particularly those with cisplatin-resistant disease.

This approach could revolutionize ovarian cancer treatment by providing a cost-effective, easily accessible option to enhance current therapies and improve patient outcomes.

Conclusion

Ovarian cancer remains a formidable challenge in oncology, mainly due to the high rates of recurrence and chemoresistance.

Mebendazole offers new hope, not just as a standalone therapy but as a synergistic agent that can enhance the effectiveness of existing treatments.

Targeting cancer cells through multiple mechanisms is a promising step toward improving ovarian cancer patients’ survival and quality of life.

Further clinical research is essential to bring this potential breakthrough from the laboratory to the bedside.

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Reference:

1. Elayapillai S, Ramraj S, Benbrook DM, Bieniasz M, Wang L, Pathuri G, Isingizwe ZR, Kennedy AL, Zhao YD, Lightfoot S, Hunsucker LA, Gunderson CC. Potential and mechanism of mebendazole for treatment and maintenance of ovarian cancer. Gynecol Oncol. 2021 Jan;160(1):302-311. doi: 10.1016/j.ygyno.2020.10.010. Epub 2020 Oct 31. PMID: 33131904; PMCID: PMC8820236.
2. Huang L, Zhao L, Zhang J, He F, Wang H, Liu Q, Shi D, Ni N, Wagstaff W, Chen C, Reid RR, Haydon RC, Luu HH, Shen L, He TC, Tang L. Antiparasitic mebendazole (MBZ) effectively overcomes cisplatin resistance in human ovarian cancer cells by inhibiting multiple cancer-associated signaling pathways. Aging (Albany NY). 2021 Jul 7;13(13):17407-17427. doi: 10.18632/aging.203232. Epub 2021 Jul 7. PMID: 34232919; PMCID: PMC8312413.

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