Newly developed MEIS inhibitor selectively blocks MEISHigh prostate cancer growth and induces apoptosis

Girgin, Birkan; Kocabaş, Fatih

doi:10.1016/j.gene.2023.147425

Gene

2023

DOI: 10.1016/j.gene.2023.147425

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Newly developed MEIS inhibitor selectively blocks MEISHigh prostate cancer growth and induces apoptosis

Birkan Girgin

Fatih Kocabaş

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2024

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Cited by 2 publications

References 48 publications

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Myeloid ectopic viral integration site 2 accelerates the progression of Alzheimer's disease

Cui,

Zhang,

Liu

et al. 2024

Aging Cell

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Amyloid plaques, a major pathological hallmark of Alzheimer's disease (AD), are caused by an imbalance between the amyloidogenic and non‐amyloidogenic pathways of amyloid precursor protein (APP). BACE1 cleavage of APP is the rate‐limiting step for amyloid‐β production and plaque formation in AD. Although the alteration of BACE1 expression in AD has been investigated, the underlying mechanisms remain unknown. In this study, we determined MEIS2 was notably elevated in AD models and AD patients. Alterations in the expression of MEIS2 can modulate the levels of BACE1. MEIS2 downregulation improved the learning and memory retention of AD mice and decreased the number of amyloid plaques. MEIS2 binds to the BACE1 promoter, positively regulates BACE1 expression, and accelerates APP amyloid degradation in vitro. Therefore, our findings suggest that MEIS2 might be a critical transcription factor in AD, since it regulates BACE1 expression and accelerates BACE1‐mediated APP amyloidogenic cleavage. MEIS2 is a promising early intervention target for AD treatment.

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Myeloid ectopic viral integration site 2 accelerates the progression of Alzheimer's disease

Cui,

Zhang,

Liu

et al. 2024

Aging Cell

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Development, synthesis and validation of improved c‐Myc/Max inhibitors

Yıldırım,

Kocabaş,

Mermer

2024

J Cellular Molecular Medi

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The pathophysiological foundations of various diseases are often subject to alteration through the utilization of small compounds, rendering them invaluable tools for the exploration and advancement of novel therapeutic strategies. Within the scope of this study, we meticulously curated a diverse library of novel small compounds meticulously designed to specifically target the c‐Myc/Max complex. We conducted in vitro examinations of novel c‐Myc inhibitors across a spectrum of cancer cell lines, including PANC1 (pancreatic adenocarcinoma), MCF7 (breast carcinoma), DU‐145 (prostate carcinoma), and A549 (lung cancer). The initial analysis involved a 25 μM dose, which enabled the identification of potent anticancer compounds effective against a variety of tumour types. We identified c‐Myc inhibitors with remarkable potency, featuring IC50 values as low as 1.6 μM and up to 40 times more effective than the reference molecule in diminishing cancer cell viability. Notably, c‐Myc‐i7 exhibited exceptional selectivity, displaying 37‐fold and 59‐fold preference for targeting prostate and breast cancers, respectively, over healthy cells. Additionally, we constructed drug‐likeness models. This study underscores the potential for in vitro investigations of various tumour types using novel c‐Myc inhibitors to yield ground‐breaking and efficacious anticancer compounds.

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Newly developed MEIS inhibitor selectively blocks MEISHigh prostate cancer growth and induces apoptosis

Cited by 2 publications

References 48 publications

Myeloid ectopic viral integration site 2 accelerates the progression of Alzheimer's disease

Myeloid ectopic viral integration site 2 accelerates the progression of Alzheimer's disease

Development, synthesis and validation of improved c‐Myc/Max inhibitors

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