Based on the studies suggesting efficacy in prophylaxis combined with the known safety profile of ivermectin, a citywide prevention program using ivermectin for COVID-19 was implemented in Itaja, a southern . . Dominguez-Gomez G., Chavez-Blanco A., Medina-Franco J.L., Saldivar-Gonzalez F., Flores-Torrontegui Y., Juarez M., Diaz-Chavez J., Gonzalez-Fierro A., Duenas-Gonzalez A. Ivermectin as an inhibitor of cancer stemlike cells. Caly L., Druce J.D., Catton M.G., Jans D.A., Wagstaff K.M. Yang J.D., Hainaut P., Gores G.J., Amadou A., Plymoth A., Roberts L.R. Jiang L., Wang P., Sun Y.J., Wu Y.J. Ivermectin proposes many potentials effects to treat a range of diseases, with its antimicrobial, antiviral, and anti-cancer properties as a wonder drug. Cancer cells exposure to IVM can be induced to generate ROS generation and reduce membrane potential of mitochondria. It included data from Surgisphere, a company that also provided inaccurate patient data . Ivermectin is a macrolide antiparasitic drug with a 16-membered ring that is widely used for the treatment of many parasitic diseases such as river blindness, elephantiasis and scabies. Although there is currently little evidences showing that IVM induces pyroptosis, it is important to investigate the role of IVM in inducing pyroptosis in other cancers in future studies and realize that IVM may induce different types of programmed cell death in different types of cancer. IVM can promote ROS release in cancer cells by P2 4/P2 7 receptors. We found that the anticancer . Ivermectin is an anthelmintic. Targeting PAK1 is a novel and promising method for cancer treatment, and the development of PAK1 inhibitors has attracted widespread attention [111]. Han S.J., Lovaszi M., Kim M., DAgati V., Hasko G., Lee H.T. In addition, characteristic pyroptosis phenomena such as cell swelling and rupturing were observed. cancer, HIV or AIDS, . Autophagy is a lysosomal-dependent form of programmed cell death. Its morbidity has increased by an average of 2% annually worldwide and the clinical treatment effect is not satisfactory [[45], [46], [47]]. IVM regulates the tumor microenvironment and mediates immunogenic cell death, which may be a new direction for research exploring anticancer mechanisms in the future. 88]. Written by Carolyn Crist. The mechanism was related to the increase in the influx of chloride ions into the cell by IVM, resulting in hyperpolarization of the plasma membrane and induction of reactive oxygen species (ROS) production. Ivermectin is proven to treat a variety of different cancers. In Jiang's experiment, IVM reversed the drug resistance of the vincristine-resistant colorectal cancer cell line HCT-8, doxorubicin-resistant breast cancer cell line MCF-7 and the chronic myelogenous leukemia cell line K562 [104]. Kodama M., Kodama T., Newberg J.Y., Katayama H., Kobayashi M., Hanash S.M., Yoshihara K., Wei Z., Tien J.C., Rangel R., Hashimoto K., Mabuchi S., Sawada K., Kimura T., Copeland N.G., Jenkins N.A. Mastrangelo E., Pezzullo M., De Burghgraeve T., Kaptein S., Pastorino B., Dallmeier K., de Lamballerie X., Neyts J., Hanson A.M., Frick D.N., Bolognesi M., Milani M. Ivermectin is a potent inhibitor of flavivirus replication specifically targeting NS3 helicase activity: new prospects for an old drug. I can't find ivermectin tablets anywhere. Introduction. Earlier, we mentioned that IVM combined with conventional chemotherapeutic drugs such as cisplatin [60], paclitaxel [59], daunorubicin and cytarabine [51], or with targeted drugs such as dasatinib [53] and dapafenib [73] shows great potential for cancer treatment. The relationship between apoptosis and autophagy is very complicated, and the cross talk between the two plays a vital role in the development of cancer [82]. Nishio M., Sugimachi K., Goto H., Wang J., Morikawa T., Miyachi Y., Takano Y., Hikasa H., Itoh T., Suzuki S.O., Kurihara H., Aishima S., Leask A., Sasaki T., Nakano T., Nishina H., Nishikawa Y., Sekido Y., Nakao K., Shin-Ya K., Mimori K., Suzuki A. Dysregulated YAP1/TAZ and TGF-beta signaling mediate hepatocarcinogenesis in Mob1a/1b-deficient mice. Guadalupe evaluated the effect of IVM on CSCs in the breast cancer cell line MDA-MB-231 [95]. The drug, Ivermectin, an antiparasitic medicine, is an inhibitor of the virus SARS-CoV-2 in-vitro and can effectively cause a reduction in virus at 48 hours in cell cultures. PAK1 cross regulate multiple signal pathways. 4), but there is no specific evidence to prove this speculation. Liu X., Zhang Z., Ruan J., Pan Y., Magupalli V.G., Wu H., Lieberman J. Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores. Udensi U.K., Fagbenro-Beyioku A.F. 109,110]. Thanh Huong P., Gurshaney S., Thanh Binh N., Gia Pham A., Hoang Nguyen H., Thanh Nguyen X., Pham-The H., Tran P.T., Truong Vu K., Xuan Duong N., Pelucchi C., La Vecchia C., Boffetta P., Nguyen H.D., Luu H.N. Recent studies have also found that IVM could promote the death of tumor cells by regulating the tumor microenvironment in breast cancer. Last. This medicine is available only with your doctor's . Levy J.M.M., Towers C.G., Thorburn A. It is considered as a new target for cancer therapy [107]. Interestingly, in ischemia-reperfusion experiments, IVM aggravated renal ischemia via the P2 7/NLRP3 pathway and increased the release of proinflammatory cytokines in human proximal tubular cells [ It utilizes lysosomes to eliminate superfluous or damaged organelles in the cytoplasm to maintain homeostasis. Franklin K.M., Asatryan L., Jakowec M.W., Trudell J.R., Bell R.L., Davies D.L. Liu Y., Fang S., Sun Q., Liu B. Anthelmintic drug ivermectin inhibits angiogenesis, growth and survival of glioblastoma through inducing mitochondrial dysfunction and oxidative stress. A new study evaluated the effect of ivermectin on time to recovery from coronavirus disease 2019 (COVID-19) in patients with mild to moderate disease. IVM promotes degradation of PAK1 by ubiquitination/proteasome pathway, thereby inhibiting the Akt/mTOR signaling pathway. Effect of ivermectin on Trypanosoma brucei brucei in experimentally infected mice. The combination of drugs can effectively increase efficacy, reduce toxicity or delay drug resistance. Zanconato F., Cordenonsi M., Piccolo S. YAP and TAZ: a signalling hub of the tumour microenvironment. Interestingly, ivermectin can also inhibit tumor stem cells and reverse multidrug resistance and exerts the optimal effect when used in combination with other chemotherapy drugs. Experiments showed that IVM inhibited the proliferation of human glioblastoma U87 and T98 G cells in a dose-dependent manner and induced apoptosis in a caspase-dependent manner [63]. Retweets. Over 25 Years of Clinical Experience With Ivermectin: An Overview of Safety for an Increasing Number of Indications. Drugs targeting BRAF mutations such as vemurafenib, dabrafenib and PD-1 monoclonal antibodies, including pembrolizumab and nivolumab have greatly improved the prognosis of melanoma [71,72]. The authors speculated that IVM may mediate the occurrence of pyroptosis via the P2 4/P2 7/NLRP3 pathway (Fig. Wagstaff K.M., Sivakumaran H., Heaton S.M., Harrich D., Jans D.A. ATP binding transport family-mediated drug efflux and overexpression of P-glycoprotein (P-gp) are widely considered to be the main causes of tumor MDR [[98], [99], [100]]. Consequently, we have concentrated on discussing the role of PAK1 kinase and cross-talk between various pathways and PAK1 to provide new perspectives on the mechanism of IVM function. Juarez M., Schcolnik-Cabrera A., Duenas-Gonzalez A. DEAD-box RNA helicase DDX23 modulates glioma malignancy via elevating miR-21 biogenesis. Therefore, combination therapy is the most common method of chemotherapy. It was also proven that IVM has a synergistic effect with cytarabine and daunorubicin on the treatment of leukemia. 36. Experiments confirmed that IVM could significantly inhibit the proliferation of five renal cell carcinoma cell lines without affecting the proliferation of normal kidney cells, and its mechanism may be related to the induction of mitochondrial dysfunction [48]. Lim S.M., Syn N.L., Cho B.C., Soo R.A. Acquired resistance to EGFR targeted therapy in non-small cell lung cancer: Mechanisms and therapeutic strategies. Bao S., Wu Q., McLendon R.E., Hao Y., Shi Q., Hjelmeland A.B., Dewhirst M.W., Bigner D.D., Rich J.N. Drug repositioning is a shortcut to accelerate the development of anticancer drugs. Yan S., Ci X., Chen N., Chen C., Li X., Chu X., Li J., Deng X. Anti-inflammatory effects of ivermectin in mouse model of allergic asthma. Antoszczak M., Markowska A., Markowska J., Huczynski A. Existing research is sufficient to demonstrate the great potential of IVM and its prospects as a novel promising anticancer drug after additional research. And to many, the claims simply seem implausible. It can be triggered by two activation pathways: the endogenous endoplasmic reticulum stress/mitochondrial pathway and the exogenous death receptor pathway [75,76]. JAMA Internal Medicine February 18, 2022. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. Patel H., Yacoub N., Mishra R., White A., Long Y., Alanazi S., Garrett J.T. Gasdermin D(GSDMD)is a substrate for activated caspase-1 and is considered to be a key protein in the execution of pyroptosis [86,87]. In a study by Hashimoto, it found that IVM inhibited the proliferation of various ovarian cancer cell lines, and the mechanism was related to the inhibition of PAK1 kinase [58]. Received 2020 Jun 5; Revised 2020 Sep 11; Accepted 2020 Sep 11. In addition, IVM regulated the expression of the epithelial mesenchymal-transition (EMT) related gene E-cadherin to restore the sensitivity of TNBC cells to tamoxifen, which implies the possibility that IVM functions as an epigenetic regulator in the treatment of cancer[36]. A clinical trial of 476 patients found ivermectin didn't improve the recovery time in patients who had COVID-19. This was related to the induction of mitochondrial dysfunction and oxidative stress. Liu J., Zhang K., Cheng L., Zhu H., Xu T. Progress in Understanding the Molecular Mechanisms Underlying the Antitumour Effects of Ivermectin. Diana A., Carlino F., Franzese E., Oikonomidou O., Criscitiello C., De Vita F., Ciardiello F., Orditura M. Early Triple Negative Breast Cancer: Conventional Treatment and Emerging Therapeutic Landscapes. Additionally, it has been confirmed that PAK1 is the key target of IVM that mediates its anti-melanoma activity, and IVM can also significantly reduce the lung metastasis of melanoma in animal experiments. Arcangeli S., Pinzi V., Arcangeli G. Epidemiology of prostate cancer and treatment remarks. Inflammasomes initiate the conversion of pro-caspase-1 via self-shearing into activated caspase-1. RAS activation directly initiates PAK1, MAPK and PI3K/Akt pathway. The authors report no declarations of interest. Kircik L.H., Del Rosso J.Q., Layton A.M., Schauber J. In Nappi's experiment, it was found that IVM could enhance the drug activity of the anti-androgen drug enzalutamide in the prostate cancer cell line LNCaP and reverse the resistance of the prostate cancer cell line PC3 to docetaxel [50]. Ivermectin induces apoptosis and autophagy is mutually regulated. Despite the fact that these trials found ivermectin inferior to the cream it was being tested against, it still won approval due to its low cost and ease of administration. In a study using mouse models of pancreatic cancer, the researchers found that in fact, PD-L1 is not highly expressed on pancreatic cancer cells. Therefore, IVM should be used in combination with other drugs to achieve the best effect, while the specific medication plan used to combine IVM with other drugs remains to be explored. In short, the relationship between IVM-induced apoptosis and autophagy involves a complex regulatory mechanism, and the specific molecular mechanism needs further study. In melanoma and nasopharyngeal carcinoma, IVM inhibited cell proliferation activity by inhibiting PAK1 to downregulate the expression of MEK 1/2 and ERK1/2 [69,73]. Zhu M., Li Y., Zhou Z. These participants received packages at their residences that contained either a dose of ivermectin or a placebo. However, here, we must emphasize that because IVM cannot effectively pass the blood-brain barrier [67], the prospect of the use of IVM in the treatment of gliomas is not optimistic. 1-26 However, those studies have limitations that make them less definitive and informative than the studies summarized in the table. Executive Summary. However, NAC reversed the effect of IVM, which indicated that IVM increased TFE3-dependent autophagy through the ROS signaling pathway. This proves that IVM mainly exerts an antitumor effect through the autophagy pathway. Yin J., Park G., Lee J.E., Choi E.Y., Park J.Y., Kim T.H., Park N., Jin X., Jung J.E., Shin D., Hong J.H., Kim H., Yoo H., Lee S.H., Kim Y.J., Park J.B., Kim J.H. HSP27 is a molecular chaperone protein that is highly expressed in many cancers and associated with drug resistance and poor prognosis. IVM could significantly reduce the mitochondrial membrane potential and inhibit mitochondrial respiration and ATP production. An experiment found that IVM could significantly enhance the inhibitory effects of erlotinib and cetuximab on lung cancer and colorectal cancer [50]. Identifying the predominant or most important contributor to cell death in each cancer type and environment will be crucial in determining the effectiveness of IVM-based treatments. Ivermectin reverses the drug resistance in cancer cells through EGFR/ERK/Akt/NF-kappaB pathway. Ivermectin has been used off-label widely since the original in vitro study by Caly et al. Types of Cancer Treatment; Side Effects of Cancer Treatment; Clinical Trials Information. Summary of the anticancer mechanism of IVM. PAK1 is at the junction of these pathways. Laing R., Gillan V., Devaney E. Ivermectin - Old Drug, New Tricks? This work was supported by the Science Research Innovation Team Project of Anhui Colleges and Universities (2016-40), the Bengbu City Natural Science Foundation (2019-12), the Key Projects of Science Research of Bengbu Medical College (BYKY2019009ZD) and National University Students Innovation and Entrepreneurship Training Program (201910367001). In gliomas, miR-21 can regulate the Ras/MAPK signaling pathway and enhance its effects on proliferation and invasion [65]. In addition, researchers also used the Akt activator CA-Akt to prove that IVM mainly induces autophagy by inhibiting the phosphorylation of Akt and mTOR (Fig. Giving ivermectin with balstilimab may increase the effect of balstilimab in shrinking tumors in patients with triple negative breast cancer. Wang's experiment found that IVM could selectively induce mitochondrial dysfunction and oxidative stress, causing chronic myeloid leukemia K562 cells to undergo increased caspase-dependent apoptosis compared with normal bone marrow cells [53]. Deng F., Xu Q., Long J., Xie H. Suppressing ROSTFE3dependent autophagy enhances ivermectininduced apoptosis in human melanoma cells. The PAK1-Stat3 Signaling Pathway Activates IL-6 Gene Transcription and Human Breast Cancer Stem Cell Formation. Cellular ROS can activate NLRP3 Inflammasome including ASC, NLRP3 and pro-caspase-1 assemble. Jan 9, 2023. IVM has been proven to significantly inhibit the proliferation and migration of HeLa cells and promote apoptosis [56]. Ivermectin is used to treat river blindness (onchocerciasis), intestinal infection from threadworms (strongyloidiasis), and other kinds of worm infections. Although CSCs are similar to stem cells in terms of function, because of the lack of a negative feedback regulation mechanism for stem cell self-renewal, their powerful proliferation and multidirectional differentiation abilities are unrestricted, which allows CSCs to maintain certain activities during chemotherapy and radiotherapy [[90], [91], [92]]. (3) It has become increasingly clear that IVM can induce a mixed cell death mode involving apoptosis, autophagy and pyroptosis depending on the cell conditions and cancer type. The discoverers of IVM, Japanese scientist Satoshi mura and Irish scientist William C. Campbell, won the Nobel Prize in Physiology or Medicine in 2015 [7,8]. Colorectal cancer (CRC) is the third most common cancer worldwide and still lacks effective therapy. Ivermectin, a potential anticancer drug derived from an antiparasitic drug. The secondary objectives of the study include evaluating the following efficacy outcomes: objective response rate (ORR), progression free survival (PFS), overall survival (OS), duration of response (DOR . It is characterized by double-layered or multilayered vacuolar structures containing cytoplasmic components, which are known as autophagosomes [77]. describing ivermectin activity against SARS-CoV-2, 22 and in Brazil, in particular, the use of ivermectin . Not only does IVM not overlap with other therapies in term of its mechanism of action, but the fact that of IVM has multiple targets suggests that it is not easy to produce IVM resistance. Intuyod K., Hahnvajanawong C., Pinlaor P., Pinlaor S. Anti-parasitic Drug Ivermectin Exhibits Potent Anticancer Activity Against Gemcitabine-resistant Cholangiocarcinoma In Vitro. Interestingly, IVM also restored the sensitivity of the triple-negative breast cancer to the anti-estrogen drug tamoxifen [36], which also implies the potential for IVM to be used in endocrine therapy. Pouliot J.F., LHeureux F., Liu Z., Prichard R.K., Georges E. Reversal of P-glycoprotein-associated multidrug resistance by ivermectin. Hence several favorable signals were detected in a study with several structural biases against ivermectin. There are still some problems that need to be studied and resolved before IVM is used in the clinic. In the past year, more than one million patients with gastric cancer have been diagnosed worldwide [38]. MDR of tumor cells is the main cause of relapses and deaths after chemotherapy [97]. The present study represents the first study evaluating the anticancer efficacy of ivermectin in pancreatic cancer. Degterev A., Yuan J. 1 Relatively safe. The 5-year survival rate after diagnosis is approximately 47% [27,57]. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. Li X., Lewis M.T., Huang J., Gutierrez C., Osborne C.K., Wu M.F., Hilsenbeck S.G., Pavlick A., Zhang X., Chamness G.C., Wong H., Rosen J., Chang J.C. Intrinsic resistance of tumorigenic breast cancer cells to chemotherapy. Geyer J., Gavrilova O., Petzinger E. Brain penetration of ivermectin and selamectin in mdr1a,b P-glycoprotein- and bcrp- deficient knockout mice. PAK1 can induce MEK1/2 and ERK1/2 activation by RAF and increase PI3K/Akt signaling by PDK1. 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