Methyl 5-[(1H-indol-3-yl)selanyl]-1H-benzoimidazol-2-ylcarbamate (M-24), a novel tubulin inhibitor, causes G2/M arrest and cell apoptosis by disrupting tubulin polymerization in human cervical and breast cancer cells

Zuo, Daiying; Jiang, Xuewei; Han, Meihua; Shen, Jiwei; Lang, Binyue; Guan, Qı; Bai, Zhaoshi; Han, Chunming; Li, Zengqiang; Zhang, Weige; Wu, Yingliang

doi:10.1016/j.tiv.2017.04.019

Cited by 11 publications

(5 citation statements)

References 41 publications

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“…In addition, sulfiredoxin was demonstrated to be an oncoprotein in CC and promote CC metastasis by activating the Wnt/β-catenin signaling. Sulfiredoxin was suggested to be a therapeutic target for CC [21]. ER-α36 was reported to mediate estrogen-stimulated MAPK/ERK activation as well as regulate the migration, invasion, and proliferation in CC cells [22].…”

Section: Discussionmentioning

confidence: 99%

“…A novel tubulin inhibitor, M-24, caused apoptosis through disrupting microtubule assembly and inducing cell cycle arrest in HeLa cells and MCF-7 cells. Therefore, M-24 was suggested to be a promising microtubule-destabilizing agent that has great potential for the therapeutics of cervical and breast cancers [21]. However, studies on how exosomes affect CC migration are still lacking.…”

Section: Discussionmentioning

confidence: 99%

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Mifepristone Inhibits the Migration of Cervical Cancer Cells by Inhibiting Exocrine Secretion

Sang¹,

Wang²,

Zhao³

2018

Pharmacology

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Cervical cancer (CC) is one of the most common gynecological malignancies, and metastasis limits the use of surgical resection. Metapristone (MIF) was reported to suppress the proliferation and migration of several cancer cells. Exosomes play a variety of roles in cellular biological processes. The relation of exosomes and CC is less studied. Cell viability, apoptosis assay and migration assay was conducted in HeLa cells treated by MIF by CCK-8 kit, staining by Annexin V-fluorescein isothiocyanate and propidium iodide, and wound test respectively. ISG15 expression level was examined in MIF-treated HeLa cells by Western blot. The migration of HeLa cells treated by MIF/GW4869 was measured by wound test. MIF suppressed the growth and migration, as well as induced apoptosis of CC cells. MIF inhibited the exocrine secretion of CC cells by upregulating ISG15, while treating CC cells by ISG15 stimulus, IFN, inhibited the secretion of exosomes. The inhibition of exocrine secretion by GW4869 enhanced the migration inhibition of MIF on CC cells. This study demonstrates that MIF suppresses the CC cell migration by inhibiting exocrine secretion through upregulating ISG1.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Mifepristone Inhibits the Migration of Cervical Cancer Cells by Inhibiting Exocrine Secretion

Sang¹,

Wang²,

Zhao³

2018

Pharmacology

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“…and Zhang at al. [ 39 , 40 ]. The subG0/G1 arrest suggests that the initiation of cell cycle arrest may be responsible for the antiproliferative potential.…”

Section: Resultsmentioning

confidence: 99%

Novel 7-Chloro-4-aminoquinoline-benzimidazole Hybrids as Inhibitors of Cancer Cells Growth: Synthesis, Antiproliferative Activity, in Silico ADME Predictions, and Docking

et al. 2023

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In this study, new 7-chloro-4-aminoquinoline-benzimidazole compounds were synthesized and characterized by NMR, MS, and elemental analysis. These novel hybrids differ in the type of linker and in the substituent on the benzimidazole moiety. Their antiproliferative activities were evaluated on one non-tumor (MDCK1) and seven selected tumor (CaCo-2, MCF-7, CCRF-CEM, Hut78, THP-1, and Raji) cell lines by MTT test and flow cytometry analysis. The compounds with different types of linkers and an unsubstituted benzimidazole ring, 5d, 8d, and 12d, showed strong cytotoxic activity (the GI50 ranged from 0.4 to 8 µM) and effectively suppressed the cell cycle progression in the leukemia and lymphoma cells. After 24 h of treatment, compounds 5d and 12d induced the disruption of the mitochondrial membrane potential as well as apoptosis in HuT78 cells. The drug-like properties and bioavailability of the compounds were calculated using the Swiss ADME web tool, and a molecular docking study was performed on tyrosine-protein kinase c-Src (PDB: 3G6H). Compound 12d showed good solubility and permeability and bound to c-Src with an energy of −119.99 kcal/mol, forming hydrogen bonds with Glu310 and Asp404 in the active site and other residues with van der Waals interactions. The results suggest that compound 12d could be a leading compound in the further design of effective antitumor drugs.

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“…When anti-tumor agents exert their action, apoptosis is triggered. Researches showed that those biomolecular derivatives activated apoptosis via both intrinsic (mitochondrial) and extrinsic (Fas receptor) pathways by inducing G2/M phase cell cycle arrest and downregulating E6 and E7 oncogene expression in cervical cancer cells ( 40 , 41 ).…”

Section: Novel Agents For Cervical Cancer Treatment At Preclinical Stagementioning

confidence: 99%

An Overview of Novel Agents for Cervical Cancer Treatment by Inducing Apoptosis: Emerging Drugs Ongoing Clinical Trials and Preclinical Studies

Liu

Wang

et al. 2021

Front. Med.

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As the leading cause of cancer death, cervical cancer ranks fourth for both incidence and mortality. Cervical cancer incidence and mortality rates have reportedly decreased over the last decades thanks to extensive screening and widespread vaccination against human papilloma virus. However, there have been no major improvements concerning platinum-based chemotherapy on the survival of advanced cervical cancer. Thus, novel agents are urgently needed for the improvement of therapeutic effect. With the development of molecular biology and genomics, targeted therapy research has achieved a breakthrough development, including anti-angiogenesis, immune checkpoint inhibitors, and other treatments that are efficient for treatment of cervical cancer. Apoptosis is a crucial process for tumor progression. Drugs directed at inducing tumor-cell apoptosis are regarded as important treatment modalities. Besides, a number of novel compounds synthesized or derived from plants or microorganisms exhibited prominent anti-cancer activity by changing the apoptotic balance in cervical cancer. In this review, we summarized new target therapy drugs ongoing clinical trials that are used for treatment of cervical cancer. Further, we classified novel agents with a focus on improvement of therapeutic effect pre-clinically. To summarize, we also discussed application prospects of the new uses of old drugs and drug combinations, to provide researchers with new ideas for cervical cancer treatment.

show abstract

Methyl 5-[(1H-indol-3-yl)selanyl]-1H-benzoimidazol-2-ylcarbamate (M-24), a novel tubulin inhibitor, causes G2/M arrest and cell apoptosis by disrupting tubulin polymerization in human cervical and breast cancer cells

Cited by 11 publications

References 41 publications

Mifepristone Inhibits the Migration of Cervical Cancer Cells by Inhibiting Exocrine Secretion

Mifepristone Inhibits the Migration of Cervical Cancer Cells by Inhibiting Exocrine Secretion

Novel 7-Chloro-4-aminoquinoline-benzimidazole Hybrids as Inhibitors of Cancer Cells Growth: Synthesis, Antiproliferative Activity, in Silico ADME Predictions, and Docking

An Overview of Novel Agents for Cervical Cancer Treatment by Inducing Apoptosis: Emerging Drugs Ongoing Clinical Trials and Preclinical Studies

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