Literature review: treatment design to overcome anticancer drug resistance
Abstract
One of the main causes of death in the world today is cancer. Chemotherapy is one treatment that cancer patients may utilize. Anticancer medication resistance, which might forecast a rise in treatment failure rates among cancer patients, poses a challenge to the current use of anticancer treatments. Numerous investigators have studied potential approaches to combat anti-cancer medication resistance. The purpose of this literature review is to provide information on treatment planning that can be applied to counteract anti-cancer medication resistance. Cancer is one of the leading causes of death in the modern world. One therapeutic option available to cancer patients is chemotherapy. The current usage of anticancer medicines is challenged by anticancer medication resistance, which may predict an increase in treatment failure rates among cancer patients. Many researchers have looked into possible strategies to fight drug resistance to anti-cancer medications. This review of the literature aims to give information on treatment planning that can be used to combat drug resistance to anti-cancer medications.
References
[1] R. L. Siegel, K. D. Miller, H. E. Fuchs, and A. Jemal, “Cancer statistics, 2022,” CA. Cancer J. Clin., vol. 72, no. 1, pp. 7–33, 2022, doi: 10.3322/caac.21708.
[2] H. Sung et al., “Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries,” CA. Cancer J. Clin., vol. 71, no. 3, pp. 209–249, 2021, doi: 10.3322/caac.21660.
[3] R. K. Kankala et al., “Overcoming Multidrug Resistance through the Synergistic Effects of Hierarchical pH-Sensitive, ROS-Generating Nanoreactors,” ACS Biomater. Sci. Eng., vol. 3, no. 10, pp. 2431–2442, 2017, doi: 10.1021/acsbiomaterials.7b00569.
[4] T. Li et al., “Glioma diagnosis and therapy: Current challenges and nanomaterial-based solutions,” J. Control.
Release, vol. 352, pp. 338–370, 2022, doi: https://doi.org/10.1016/j.jconrel.2022.09.065.
[5] WHO, “Cancer : Overview,” WHO, 2022. https://www.who.int/news-room/fact-sheets/detail/cancer
[6] K. Bukowski, M. Kciuk, and R. Kontek, “Mechanisms of multidrug resistance in cancer chemotherapy1. Bukowski K, Kciuk M, Kontek R. Mechanisms of multidrug resistance in cancer chemotherapy. Int J Mol Sci. 2020;21(9). doi:10.3390/ijms21093233,” Int. J. Mol. Sci., vol. 21, no. 9, 2020.
[7] T. H. Lippert, H. J. Ruoff, and M. Volm, “Current status of methods to assess cancer drug resistance,” Int. J. Med. Sci., vol. 8, no. 3, pp. 245–253, 2011, doi: 10.7150/ijms.8.245.
[8] Y. He, P. Ji, Y. Li, R. Wang, H. Ma, and H. Yuan, “Genetic Variants Were Associated With the Prognosis of Head
and Neck Squamous Carcinoma,” Front. Oncol., vol. 10, no. March, pp. 1–8, 2020, doi: 10.3389/fonc.2020.00372.
[9] S. A. Mir et al., “Role of Nanotechnology in Overcoming the Multidrug Resistance in Cancer Therapy: A Review,” Molecules, vol. 27, no. 19, 2022, doi: 10.3390/molecules27196608.
[10] G. Housman et al., “Drug resistance in cancer: An overview,” Cancers (Basel)., vol. 6, no. 3, pp. 1769–1792, 2014, doi: 10.3390/cancers6031769.
[11] T. Ozben, “Mechanisms and strategies to overcome multiple drug resistance in cancer,” FEBS Lett., vol. 580, no. 12, pp. 2903–2909, 2006, doi: 10.1016/j.febslet.2006.02.020.
[12] J. Wang, N. Seebacher, H. Shi, Q. Kan, and Z. Duan, “Novel strategies to prevent the development of multidrug resistance (MDR) in cancer,” Oncotarget, vol. 8, no. 48, pp. 84559–84571, 2017, doi: 10.18632/oncotarget.19187.
[13] N. Saini et al., “Mutation signatures specific to DNA alkylating agents in yeast and cancers,” Nucleic Acids Res., vol. 48, no. 7, pp. 3692–3707, 2020, doi: 10.1093/NAR/GKAA150.
[14] S. Vinogradov and X. Wei, “Cancer stem cells and drug resistance: The potential of nanomedicine,” Nanomedicine, vol. 7, no. 4, pp. 597–615, 2012, doi: 10.2217/nnm.12.22.
[15] C. Duan, M. Yu, J. Xu, B. Y. Li, Y. Zhao, and R. K. Kankala, “Overcoming Cancer Multi-drug Resistance (MDR): Reasons, mechanisms, nanotherapeutic solutions, and challenges,” Biomed. Pharmacother., vol. 162, no. February, pp. 0–3, 2023, doi: 10.1016/j.biopha.2023.114643.
[16] Y. Cao et al., “Screening potential P-glycoprotein inhibitors by combination of a detergent-free membrane protein extraction with surface plasmon resonance biosensor,” Acta Pharm. Sin. B, vol. 12, no. 7, pp. 3113–3123, 2022, doi: 10.1016/j.apsb.2022.03.016.
[17] J. Dong et al., “Medicinal chemistry strategies to discover P-glycoprotein inhibitors: An update,” Drug Resist. Updat., vol. 49, no. January, p. 100681, 2020, doi: 10.1016/j.drup.2020.100681.
[18] J. I. Lai, Y. J. Tseng, M. H. Chen, C. Y. F. Huang, and P. M. H. Chang, “Clinical Perspective of FDA Approved Drugs With P-Glycoprotein Inhibition Activities for Potential Cancer Therapeutics,” Front. Oncol., vol. 10, no. November, 2020, doi: 10.3389/fonc.2020.561936.
[19] C. Seidl et al., MicroRNA-182-5p regulates hedgehog signaling pathway and chemosensitivity of cisplatin-resistant lung adenocarcinoma cells via targeting GLI2, vol. 469. Elsevier B.V., 2020. doi: 10.1016/j.canlet.2019.10.044.
[20] S. Wang, T. Lei, and M. Zhang, “The reversal effect and its mechanisms of Tetramethylpyrazine on multidrug resistance in human bladder cancer,” PLoS One, vol. 11, no. 7, pp. 1–19, 2016, doi: 10.1371/journal.pone.0157759.
[21] M. Wang, T. R. Moore, J. Talbot, and J. L. Riley, “Global Biogeochemical Cycles in peat formation,” Global Biogeochem. Cycles, pp. 113–121, 2014, doi: 10.1002/2014GB005000.Received.
[22] J. Dartier et al., “ATP-dependent activity and mitochondrial localization of drug efflux pumps in doxorubicin-resistant breast cancer cells,” Biochim. Biophys. Acta - Gen. Subj., vol. 1861, no. 5, pp. 1075–1084, 2017, doi: 10.1016/j.bbagen.2017.02.019.
[23] Y. Liu, X. Zhang, M. Zhou, X. Nan, X. Chen, and X. Zhang, “Mitochondrial-Targeting Lonidamine-Doxorubicin Nanoparticles for Synergistic Chemotherapy to Conquer Drug Resistance,” ACS Appl. Mater. Interfaces, vol. 9, no. 50, pp. 43498–43507, 2017, doi: 10.1021/acsami.7b14577.
[24] H. Yu et al., “Tumor acidity activated triphenylphosphonium-based mitochondrial targeting nanocarriers for overcoming drug resistance of cancer therapy,” Theranostics, vol. 9, no. 23, pp. 7033–7050, 2019, doi: 10.7150/thno.35748.
[25] W. Zhou et al., “Redox-triggered activation of nanocarriers for mitochondria-targeting cancer chemotherapy,” Nanoscale, vol. 9, no. 43, pp. 17044–17053, 2017, doi: 10.1039/c7nr06130g.
[26] L. Xiang et al., “HIF-1-dependent heme synthesis promotes gemcitabine resistance in human non-small cell lung cancers via enhanced ABCB6 expression.,” Cell. Mol. Life Sci., vol. 79, no. 6, p. 343, Jun. 2022, doi: 10.1007/s00018-022-04360-9.
[27] N. Albadari, S. Deng, and W. Li, “The transcriptional factors HIF-1 and HIF-2 and their novel inhibitors in cancer therapy,” Expert Opin. Drug Discov., vol. 14, no. 7, pp. 667–682, 2019, doi: 10.1080/17460441.2019.1613370.
[28] K. Luo et al., “Reduction-sensitive platinum (IV)-prodrug nano-sensitizer with an ultra-high drug loading for efficient chemo-radiotherapy of Pt-resistant cervical cancer in vivo,” J. Control. Release, vol. 326, no. Iv, pp. 25–37, 2020, doi: 10.1016/j.jconrel.2020.06.005.
[29] Z. Ma et al., “Targeting hypoxia-inducible factor-1, for cancer treatment: Recent advances in developing small-molecule inhibitors from natural compounds,” Semin. Cancer Biol., vol. 80, pp. 379–390, 2022, doi: 10.1016/j.semcancer.2020.09.011.
[30] R. Weijer et al., “Inhibition of hypoxia inducible factor 1 and topoisomerase with acriflavine sensitizes perihilar cholangiocarcinomas to photodynamic therapy,” Oncotarget, vol. 7, no. 3, pp. 3341–3356, 2016, doi: 10.18632/oncotarget.6490.
[31] X. Zhang et al., “One-pot synthesis of a microporous organosilica-coated cisplatin nanoplatform for HIF-1-targeted combination cancer therapy,” Theranostics, vol. 10, no. 7, pp. 2918–2929, 2020, doi: 10.7150/thno.41077.
[32] L. Zhang et al., “Clinical characteristics of COVID-19-infected cancer patients: a retrospective case study in three hospitals within Wuhan, China,” Ann. Oncol., vol. 31, no. 7, pp. 894–901, 2020, doi: 10.1016/j.annonc.2020.03.296.
[33] T. Stiewe and T. E. Haran, “How mutations shape p53 interactions with the genome to promote tumorigenesis and drug resistance,” Drug Resist. Updat., vol. 38, no. 2010, pp. 27–43, 2018, doi: 10.1016/j.drup.2018.05.001.
[34] J. Haldrup et al., “FRMD6 has tumor suppressor functions in prostate cancer,” Oncogene, vol. 40, no. 4, pp. 763–776, 2021, doi: 10.1038/s41388-020-01548-w.
[35] L. Gao, Z. X. Wu, Y. G. Assaraf, Z. S. Chen, and L. Wang, “Overcoming anti-cancer drug resistance via restoration of tumor suppressor gene function,” Drug Resist. Updat., vol. 57, no. January, p. 100770, 2021, doi: 10.1016/j.drup.2021.100770.
[36] J. E. Lee and M. Y. Kim, “Cancer epigenetics: Past, present and future,” Semin. Cancer Biol., vol. 83, no. January, pp. 4–14, 2022, doi: 10.1016/j.semcancer.2021.03.025.
[37] Z. Lin et al., “ RNA m 6 A methylation regulates sorafenib resistance in liver cancer through FOXO 3‐mediated autophagy ,” EMBO J., vol. 39, no. 12, pp. 1–19, 2020, doi: 10.15252/embj.2019103181.
[2] H. Sung et al., “Global Cancer Statistics 2020: GLOBOCAN Estimates of Incidence and Mortality Worldwide for 36 Cancers in 185 Countries,” CA. Cancer J. Clin., vol. 71, no. 3, pp. 209–249, 2021, doi: 10.3322/caac.21660.
[3] R. K. Kankala et al., “Overcoming Multidrug Resistance through the Synergistic Effects of Hierarchical pH-Sensitive, ROS-Generating Nanoreactors,” ACS Biomater. Sci. Eng., vol. 3, no. 10, pp. 2431–2442, 2017, doi: 10.1021/acsbiomaterials.7b00569.
[4] T. Li et al., “Glioma diagnosis and therapy: Current challenges and nanomaterial-based solutions,” J. Control.
Release, vol. 352, pp. 338–370, 2022, doi: https://doi.org/10.1016/j.jconrel.2022.09.065.
[5] WHO, “Cancer : Overview,” WHO, 2022. https://www.who.int/news-room/fact-sheets/detail/cancer
[6] K. Bukowski, M. Kciuk, and R. Kontek, “Mechanisms of multidrug resistance in cancer chemotherapy1. Bukowski K, Kciuk M, Kontek R. Mechanisms of multidrug resistance in cancer chemotherapy. Int J Mol Sci. 2020;21(9). doi:10.3390/ijms21093233,” Int. J. Mol. Sci., vol. 21, no. 9, 2020.
[7] T. H. Lippert, H. J. Ruoff, and M. Volm, “Current status of methods to assess cancer drug resistance,” Int. J. Med. Sci., vol. 8, no. 3, pp. 245–253, 2011, doi: 10.7150/ijms.8.245.
[8] Y. He, P. Ji, Y. Li, R. Wang, H. Ma, and H. Yuan, “Genetic Variants Were Associated With the Prognosis of Head
and Neck Squamous Carcinoma,” Front. Oncol., vol. 10, no. March, pp. 1–8, 2020, doi: 10.3389/fonc.2020.00372.
[9] S. A. Mir et al., “Role of Nanotechnology in Overcoming the Multidrug Resistance in Cancer Therapy: A Review,” Molecules, vol. 27, no. 19, 2022, doi: 10.3390/molecules27196608.
[10] G. Housman et al., “Drug resistance in cancer: An overview,” Cancers (Basel)., vol. 6, no. 3, pp. 1769–1792, 2014, doi: 10.3390/cancers6031769.
[11] T. Ozben, “Mechanisms and strategies to overcome multiple drug resistance in cancer,” FEBS Lett., vol. 580, no. 12, pp. 2903–2909, 2006, doi: 10.1016/j.febslet.2006.02.020.
[12] J. Wang, N. Seebacher, H. Shi, Q. Kan, and Z. Duan, “Novel strategies to prevent the development of multidrug resistance (MDR) in cancer,” Oncotarget, vol. 8, no. 48, pp. 84559–84571, 2017, doi: 10.18632/oncotarget.19187.
[13] N. Saini et al., “Mutation signatures specific to DNA alkylating agents in yeast and cancers,” Nucleic Acids Res., vol. 48, no. 7, pp. 3692–3707, 2020, doi: 10.1093/NAR/GKAA150.
[14] S. Vinogradov and X. Wei, “Cancer stem cells and drug resistance: The potential of nanomedicine,” Nanomedicine, vol. 7, no. 4, pp. 597–615, 2012, doi: 10.2217/nnm.12.22.
[15] C. Duan, M. Yu, J. Xu, B. Y. Li, Y. Zhao, and R. K. Kankala, “Overcoming Cancer Multi-drug Resistance (MDR): Reasons, mechanisms, nanotherapeutic solutions, and challenges,” Biomed. Pharmacother., vol. 162, no. February, pp. 0–3, 2023, doi: 10.1016/j.biopha.2023.114643.
[16] Y. Cao et al., “Screening potential P-glycoprotein inhibitors by combination of a detergent-free membrane protein extraction with surface plasmon resonance biosensor,” Acta Pharm. Sin. B, vol. 12, no. 7, pp. 3113–3123, 2022, doi: 10.1016/j.apsb.2022.03.016.
[17] J. Dong et al., “Medicinal chemistry strategies to discover P-glycoprotein inhibitors: An update,” Drug Resist. Updat., vol. 49, no. January, p. 100681, 2020, doi: 10.1016/j.drup.2020.100681.
[18] J. I. Lai, Y. J. Tseng, M. H. Chen, C. Y. F. Huang, and P. M. H. Chang, “Clinical Perspective of FDA Approved Drugs With P-Glycoprotein Inhibition Activities for Potential Cancer Therapeutics,” Front. Oncol., vol. 10, no. November, 2020, doi: 10.3389/fonc.2020.561936.
[19] C. Seidl et al., MicroRNA-182-5p regulates hedgehog signaling pathway and chemosensitivity of cisplatin-resistant lung adenocarcinoma cells via targeting GLI2, vol. 469. Elsevier B.V., 2020. doi: 10.1016/j.canlet.2019.10.044.
[20] S. Wang, T. Lei, and M. Zhang, “The reversal effect and its mechanisms of Tetramethylpyrazine on multidrug resistance in human bladder cancer,” PLoS One, vol. 11, no. 7, pp. 1–19, 2016, doi: 10.1371/journal.pone.0157759.
[21] M. Wang, T. R. Moore, J. Talbot, and J. L. Riley, “Global Biogeochemical Cycles in peat formation,” Global Biogeochem. Cycles, pp. 113–121, 2014, doi: 10.1002/2014GB005000.Received.
[22] J. Dartier et al., “ATP-dependent activity and mitochondrial localization of drug efflux pumps in doxorubicin-resistant breast cancer cells,” Biochim. Biophys. Acta - Gen. Subj., vol. 1861, no. 5, pp. 1075–1084, 2017, doi: 10.1016/j.bbagen.2017.02.019.
[23] Y. Liu, X. Zhang, M. Zhou, X. Nan, X. Chen, and X. Zhang, “Mitochondrial-Targeting Lonidamine-Doxorubicin Nanoparticles for Synergistic Chemotherapy to Conquer Drug Resistance,” ACS Appl. Mater. Interfaces, vol. 9, no. 50, pp. 43498–43507, 2017, doi: 10.1021/acsami.7b14577.
[24] H. Yu et al., “Tumor acidity activated triphenylphosphonium-based mitochondrial targeting nanocarriers for overcoming drug resistance of cancer therapy,” Theranostics, vol. 9, no. 23, pp. 7033–7050, 2019, doi: 10.7150/thno.35748.
[25] W. Zhou et al., “Redox-triggered activation of nanocarriers for mitochondria-targeting cancer chemotherapy,” Nanoscale, vol. 9, no. 43, pp. 17044–17053, 2017, doi: 10.1039/c7nr06130g.
[26] L. Xiang et al., “HIF-1-dependent heme synthesis promotes gemcitabine resistance in human non-small cell lung cancers via enhanced ABCB6 expression.,” Cell. Mol. Life Sci., vol. 79, no. 6, p. 343, Jun. 2022, doi: 10.1007/s00018-022-04360-9.
[27] N. Albadari, S. Deng, and W. Li, “The transcriptional factors HIF-1 and HIF-2 and their novel inhibitors in cancer therapy,” Expert Opin. Drug Discov., vol. 14, no. 7, pp. 667–682, 2019, doi: 10.1080/17460441.2019.1613370.
[28] K. Luo et al., “Reduction-sensitive platinum (IV)-prodrug nano-sensitizer with an ultra-high drug loading for efficient chemo-radiotherapy of Pt-resistant cervical cancer in vivo,” J. Control. Release, vol. 326, no. Iv, pp. 25–37, 2020, doi: 10.1016/j.jconrel.2020.06.005.
[29] Z. Ma et al., “Targeting hypoxia-inducible factor-1, for cancer treatment: Recent advances in developing small-molecule inhibitors from natural compounds,” Semin. Cancer Biol., vol. 80, pp. 379–390, 2022, doi: 10.1016/j.semcancer.2020.09.011.
[30] R. Weijer et al., “Inhibition of hypoxia inducible factor 1 and topoisomerase with acriflavine sensitizes perihilar cholangiocarcinomas to photodynamic therapy,” Oncotarget, vol. 7, no. 3, pp. 3341–3356, 2016, doi: 10.18632/oncotarget.6490.
[31] X. Zhang et al., “One-pot synthesis of a microporous organosilica-coated cisplatin nanoplatform for HIF-1-targeted combination cancer therapy,” Theranostics, vol. 10, no. 7, pp. 2918–2929, 2020, doi: 10.7150/thno.41077.
[32] L. Zhang et al., “Clinical characteristics of COVID-19-infected cancer patients: a retrospective case study in three hospitals within Wuhan, China,” Ann. Oncol., vol. 31, no. 7, pp. 894–901, 2020, doi: 10.1016/j.annonc.2020.03.296.
[33] T. Stiewe and T. E. Haran, “How mutations shape p53 interactions with the genome to promote tumorigenesis and drug resistance,” Drug Resist. Updat., vol. 38, no. 2010, pp. 27–43, 2018, doi: 10.1016/j.drup.2018.05.001.
[34] J. Haldrup et al., “FRMD6 has tumor suppressor functions in prostate cancer,” Oncogene, vol. 40, no. 4, pp. 763–776, 2021, doi: 10.1038/s41388-020-01548-w.
[35] L. Gao, Z. X. Wu, Y. G. Assaraf, Z. S. Chen, and L. Wang, “Overcoming anti-cancer drug resistance via restoration of tumor suppressor gene function,” Drug Resist. Updat., vol. 57, no. January, p. 100770, 2021, doi: 10.1016/j.drup.2021.100770.
[36] J. E. Lee and M. Y. Kim, “Cancer epigenetics: Past, present and future,” Semin. Cancer Biol., vol. 83, no. January, pp. 4–14, 2022, doi: 10.1016/j.semcancer.2021.03.025.
[37] Z. Lin et al., “ RNA m 6 A methylation regulates sorafenib resistance in liver cancer through FOXO 3‐mediated autophagy ,” EMBO J., vol. 39, no. 12, pp. 1–19, 2020, doi: 10.15252/embj.2019103181.
Published
2024-10-31
How to Cite
UDIN, Baha et al.
Literature review: treatment design to overcome anticancer drug resistance.
JURNAL ILMU KEFARMASIAN INDONESIA, [S.l.], v. 22, n. 2, p. 282-288, oct. 2024.
ISSN 2614-6495.
Available at: <http://jifi.farmasi.univpancasila.ac.id/index.php/jifi/article/view/1573>. Date accessed: 21 nov. 2024.
doi: https://doi.org/10.35814/jifi.v22i2.1573.
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