Surveying FDA-approved drugs as new potential inhibitors of N-cadherin protein: a virtual screening approach

Khajeh, Sahar; Eslami, Mahboobeh; Nezafat, Navid; Mostafavi‐Pour, Zohreh; Negahdaripour, Manica; Ghasemi, Younes; Razban, Vahid

doi:10.1007/s11224-020-01595-9

Cited by 2 publications

(3 citation statements)

References 31 publications

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“…In fact N-cadherin contribution on generation of cell-cell junctions is less than that of E-cadherin, and its higher expression in PC3 cells is closely related to 'more mesenchymal phenotype' and increased cell invasion capacity of these cells compared with DU145 cells. 37 Based on our previous in silico studies, 15,16 we hypothesized that Tel could act as N-cadherin antagonist. Therefore, in contrast to DU145 of Tel on N-cadherin inhibition.…”

Section: Effects Of Dtx Tel and Adh-1 On Induction Of Apoptosis In Pr...mentioning

confidence: 99%

“…13 In previous in silico studies, after deep analysis of N-cadherin/ADH-1 interaction, we screened for FDA-approved small molecules which can act as potential inhibitors for N-cadherin protein. 15,16 Among seven screened candidate drugs, we decided to use one of these inhibitors, Telmisartan (Tel) in the current study. Our hypothesis was that Tel prevents cell migration and inhibits attachment of PCa and breast cancer cells to recombinant N-cadherin coated wells by suppressing N-cadherin.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, the use of new drugs with less invasiveness administration route, controllability and high bioavailability is very efficient 13 . In previous in silico studies, after deep analysis of N‐cadherin/ADH‐1 interaction, we screened for FDA‐approved small molecules which can act as potential inhibitors for N‐cadherin protein 15,16 . Among seven screened candidate drugs, we decided to use one of these inhibitors, Telmisartan (Tel) in the current study.…”

Section: Introductionmentioning

confidence: 99%

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Telmisartan anti‐cancer activities mechanism through targeting N‐cadherin by mimicking ADH‐1 function

Khorsand

Khajeh

Eslami

et al. 2022

J Cellular Molecular Medi

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This study aimed to investigate if Telmisartan as a novel N‐cadherin antagonist, can overcome cell migration of cancer cells. We investigated the mechanism and influence of Docetaxel and Telmisartan (as an analogous to ADH‐1, which is a well‐known N‐cadherin antagonist) on cancer cells. The effect of ADH‐1 and Telmisartan on cell attachment in PC3, DU145, MDA‐MB‐468 cell lines using recombinant human N‐cadherin was studied. Cell viability assay was performed to examine the anti‐proliferative effects of Telmisartan, ADH‐1 and Docetaxel. Migration was examined via wound healing assay, and apoptosis was determined by flow cytometry. The expression of AKT‐1 as a downstream gene of N‐cadherin signalling pathway was assayed by real‐time PCR. Treatment of PC3, MDA‐MB‐468 and DU145 cells with Telmisartan (0.1 µM) and ADH‐1 (40 µM) resulted in 50%, 58% and approximately 20% reduction in cell attachment to N‐cadherin coated plate respectively. It shows reduction of cell attachment in PC3 and MDA‐MB‐468 cell lines appeared to be more sensitive than that of DU145 cells to the Telmisartan and ADH‐1 treatments. Telmisartan (0.1 µM) and Docetaxel (0.01 nM) significantly reduced cell migration in PC3 and MDA‐MB‐468 cell lines compared with the control group. Using Real‐time PCR, we found that Telmisartan, Docetaxel and ADH‐1 had significant influence on the AKT‐1 mRNA level. The results of the current study for the first time suggest that, Telmisartan, exerts anti‐proliferation and anti‐migration effects by targeting antagonistically N‐cadherin. Also, these data suggest that Telmisartan as a less expensive alternative to ADH‐1 could potentiate Docetaxel anticancer effects.

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Section: Effects Of Dtx Tel and Adh-1 On Induction Of Apoptosis In Pr...mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Telmisartan anti‐cancer activities mechanism through targeting N‐cadherin by mimicking ADH‐1 function

Khorsand

Khajeh

Eslami

et al. 2022

J Cellular Molecular Medi

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D-allose: Molecular Pathways and Therapeutic Capacity in Cancer

Khajeh

Ganjavi

Koushki

et al. 2023

CMP

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Background: Despite the implementation of various cancer therapies, adequate therapeutic efficacy has not been achieved. A growing number of studies have been dedicated to the discovery of new molecules to combat refractory cancer cells efficiently. Recently, the use of a rare type of sugar, D-allose, has attracted the attention of research communities. In combination with the first-line treatment of cancers, including different types of radiotherapies and chemotherapies, D-allose has been detected with favorable complementary effects. Understanding the mechanism of therapeutic target molecules will enable us to develop new strategies for cancer patients that do not currently respond to the present therapies. Objective: We aimed to provide a review of the effects of D-allose in cancer treatment, its mechanisms of action, and gaps in this field that require more investigations. Discussion: With rare exceptions, in many cancer types, including head and neck, lung, liver, bladder, blood, and breast, D-allose consistently has exhibited anticancer activity in vitro and/or in vivo. Most of the D-allose functions are mediated through thioredoxin-interacting protein molecules. D-allose exerts its effects via reactive oxygen species regulation, cell cycle arrest, metabolic reprogramming, autophagy, apoptosis induction, and sensitizing tumors to radiotherapy and chemotherapy. Conclusion: D-allose has shown great promise for combating tumor cells with no side effects, especially in combination with first-line drugs; however, its potential for cancer therapy has not been comprehensively investigated in vitro or in vivo.

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Surveying FDA-approved drugs as new potential inhibitors of N-cadherin protein: a virtual screening approach

Cited by 2 publications

References 31 publications

Telmisartan anti‐cancer activities mechanism through targeting N‐cadherin by mimicking ADH‐1 function

Telmisartan anti‐cancer activities mechanism through targeting N‐cadherin by mimicking ADH‐1 function

D-allose: Molecular Pathways and Therapeutic Capacity in Cancer

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