ReviewThe Journal of biological chemistry2020
Enigmatic MELK: The controversy surrounding its complex role in cancer.
Review in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed.
- Proteolysis Targeting Chimeric-Based Technology in Myeloma and Lymphoma.Molecular cancer therapeutics · 2026Review
- Chalcones as multitarget modulators in non-small cell lung cancer: mechanistic insights and therapeutic perspectives.Archives of toxicology · 2026Review
- Phosphosite-specific co-regulation networks of MELK kinase: insights from integrative global phosphoproteomes.Journal, genetic engineering & biotechnology · 2026Article
- Maternal Embryonic Leucine Zipper Kinase (Biology · 2026Review
- Telomere-based Risk Model for Prognosis Prediction in Clear Cell Renal Cell Carcinoma.Current medicinal chemistry · 2026Article
- The role of MELK in cancer: mechanisms and therapeutic options.Frontiers in oncology · 2026Review
- Integrated analysis of uterine leiomyosarcoma and leiomyoma utilizing TCGA and GEO data: a WGCNA and machine learning approach.Translational cancer research · 2025Article
- Up-Regulation of MELK Promotes Cell Growth and Invasion by Accelerating G1/S Transition and Indicates Poor Prognosis in Lung Adenocarcinoma.Molecular biotechnology · 2025Article
- Targeting MELK in tumor cells and tumor microenvironment: from function and mechanism to therapeutic application.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Review
- Maternal Embryonic Leucine Zipper Kinase (MELK) as a Promising Therapeutic Target in Triple Negative Breast Cancer.Anti-cancer agents in medicinal chemistry · 2025Review
- DDX56 promotes EMT and cancer stemness via MELK-FOXM1 axis in hepatocellular carcinoma.iScience · 2024Article
- E2F1-EP300 co-activator complex potentiates immune escape in nasopharyngeal carcinoma through the mediation of MELK.Histology and histopathology · 2024Article
- MELK aggravates lung adenocarcinoma by regulating EZH2 ubiquitination and H3K27me3 histone methylation of LATS2.Journal of cellular and molecular medicine · 2024Article
- Targeting MELK improves PD-1 blockade efficiency in cervical cancer via enhancing antitumor immunity.Molecular therapy. Oncology · 2024Article
- Transcriptome and Weighted Gene Co-Expression Network Analysis for Feather Follicle Density in a Chinese Indigenous Breed.Animals : an open access journal from MDPI · 2024Article
- Spatiotemporal regulation of MELK during mitosis.Frontiers in cell and developmental biology · 2024Article
- Recapitulation of patient-specific 3D chromatin conformation using machine learning.Cell reports methods · 2023Article
- A Blood-Based Immune Gene Signature with Prognostic Significance in Localized Prostate Cancer.Cancers · 2023Article
- Maternal Embryonic Leucine Zipper Kinase is Associated with Metastasis in Triple-negative Breast Cancer.Cancer research communications · 2023Article
- AURKA, TOP2A and MELK are the key genes identified by WGCNA for the pathogenesis of lung adenocarcinoma.Oncology letters · 2023Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The Ser/Thr protein kinase MELK (maternal embryonic leucine zipper kinase) has been considered an attractive therapeutic target for managing cancer since 2005. Studies using expression analysis have indicated that MELK expression is higher in numerous cancer cells and tissues than in their normal, nonneoplastic counterparts. Further, RNAi-mediated MELK depletion impairs proliferation of multiple cancers, including triple-negative breast cancer (TNBC), and these growth defects can be rescued with exogenous WT MELK, but not kinase-dead MELK complementation. Pharmacological MELK inhibition with OTS167 (alternatively called OTSSP167) and NVS-MELK8a, among other small molecules, also impairs cancer cell growth. These collective results led to MELK being classified as essential for cancer proliferation. More recently, in 2017, the proliferation of TNBC and other cancer cell lines was reported to be unaffected by genetic CRISPR/Cas9-mediated MELK deletion, calling into question the essentiality of this kinase in cancer. To date, the requirement of MELK in cancer remains controversial, and mechanisms underlying the disparate growth effects observed with RNAi, pharmacological inhibition, and CRISPR remain unclear. Our objective with this review is to highlight the evidence on both sides of this controversy, to provide commentary on the purported requirement of MELK in cancer, and to emphasize the need for continued elucidation of the functions of MELK.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.