自引率: 2.1%
被引量: 8738
通过率: 暂无数据
审稿周期: 0.67
版面费用: 暂无数据
国人发稿量: 22
投稿须知/期刊简介:
Molecular Cancer Research publishes articles describing novel basic cancer research discoveries of broad interest to the field. Studies must be of demonstrated significance, and the journal prioritizes analyses performed at the molecular and cellular level that reveal novel mechanistic insight into pathways and processes linked to cancer risk, development, and/or progression. Areas of emphasis include all cancer-associated pathways (including cell-cycle regulation; cell death; chromatin regulation; DNA damage and repair; gene and RNA regulation; genomics; oncogenes and tumor suppressors; and signal transduction), in addition to studies describing new molecular mechanisms and interactions that support cancer phenotypes. For full consideration, primary research submissions must provide significant novel insight into existing pathway functions or address new hypotheses associated with cancer-relevant biologic questions.Molecular Cancer Research accepts submissions of primary research, review and commentary article types as well as letters to the editor. For descriptions and length requirements of the article types available to submitting authors see the Categories of Articles for Molecular Cancer Research. The AACR Journals all use a similar Editorial Process. Please note that Molecular Cancer Research does not consider appeals.Submitting authors must be familiar with the Editorial Policies of the AACR Journals covering important information on authorship, publishing ethics, availability of materials and data and data analysis and reporting.Manuscripts are stringently reviewed for high standards of scientific merit, and only those that report results of novel, timely, and broadly-significant research are accepted for publication.
期刊描述简介:
Molecular Cancer Research publishes articles describing novel basic cancer research discoveries of broad interest to the field. Studies must be of demonstrated significance, and the journal prioritizes analyses performed at the molecular and cellular level that reveal novel mechanistic insight into pathways and processes linked to cancer risk, development, and/or progression. Areas of emphasis include all cancer-associated pathways (including cell-cycle regulation; cell death; chromatin regulation; DNA damage and repair; gene and RNA regulation; genomics; oncogenes and tumor suppressors; and signal transduction), in addition to studies describing new molecular mechanisms and interactions that support cancer phenotypes. For full consideration, primary research submissions must provide significant novel insight into existing pathway functions or address new hypotheses associated with cancer-relevant biologic questions. Molecular Cancer Research accepts submissions of primary research, review and commentary article types as well as letters to the editor. For descriptions and length requirements of the article types available to submitting authors see the Categories of Articles for Molecular Cancer Research. The AACR Journals all use a similar Editorial Process. Please note that Molecular Cancer Research does not consider appeals. Submitting authors must be familiar with the Editorial Policies of the AACR Journals covering important information on authorship, publishing ethics, availability of materials and data and data analysis and reporting. Manuscripts are stringently reviewed for high standards of scientific merit, and only those that report results of novel, timely, and broadly-significant research are accepted for publication.
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The Complex Regulation of Cytokinesis upon Abscission Checkpoint Activation.
Cytokinetic abscission is a crucial process that guides the separation of daughter cells at the end of each cell division. This process involves the cleavage of the intercellular bridge, which connects the newly formed daughter cells. Over the years, researchers have identified several cellular contributors and intracellular processes that influence the spatial and temporal distribution of the cytoskeleton during cytokinetic abscission. This review presents the most important scientific discoveries that allow activation of the abscission checkpoint, ensuring a smooth and successful separation of a single cell into two cells during cell division. Here, we describe different factors, such as abscission checkpoint, ICB tension, nuclear pore defects, DNA replication stress, chromosomal stability, and midbody proteins, which play a role in the regulation and correct timing of cytokinetic abscission. Furthermore, we explore the downsides associated with the dysregulation of abscission, including its negative impact on cells and the potential to induce tumor formation in humans. Finally, we propose a novel factor for improving cancer therapy and give future perspectives in this research field.
被引量：- 发表：2024
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Ruthenium drug BOLD-100 regulates BRAFMT colorectal cancer cell apoptosis through AhR/ROS/ATR signaling axis modulation.
被引量：- 发表：1970
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GRAIL1 Stabilizes Misfolded Mutant p53 through a Ubiquitin Ligase-Independent, Chaperone Regulatory Function.
Frequent (>70%) TP53 mutations often promote its protein stabilization, driving esophageal adenocarcinoma (EAC) development linked to poor survival and therapy resistance. We previously reported that during Barrett's esophagus progression to EAC, an isoform switch occurs in the E3 ubiquitin ligase RNF128 (aka GRAIL-gene related to anergy in lymphocytes), enriching isoform 1 (hereby GRAIL1) and stabilizing the mutant p53 protein. Consequently, GRAIL1 knockdown degrades mutant p53. But, how GRAIL1 stabilizes the mutant p53 protein remains unclear. In search for a mechanism, here, we performed biochemical and cell biology studies to identify that GRAIL has a binding domain (315-PMCKCDILKA-325) for heat shock protein 40/DNAJ. This interaction can influence DNAJ chaperone activity to modulate misfolded mutant p53 stability. As predicted, either the overexpression of a GRAIL fragment (Frag-J) encompassing the DNAJ binding domain or a cell-permeable peptide (Pep-J) encoding the above 10 amino acids can bind and inhibit DNAJ-Hsp70 co-chaperone activity, thus degrading misfolded mutant p53. Consequently, either Frag-J or Pep-J can reduce the survival of mutant p53 containing dysplastic Barrett's esophagus and EAC cells and inhibit the growth of patient-derived organoids of dysplastic Barrett's esophagus in 3D cultures. The misfolded mutant p53 targeting and growth inhibitory effects of Pep-J are comparable with simvastatin, a cholesterol-lowering drug that can degrade misfolded mutant p53 also via inhibiting DNAJA1, although by a distinct mechanism. Implications: We identified a novel ubiquitin ligase-independent, chaperone-regulating domain in GRAIL and further synthesized a first-in-class novel misfolded mutant p53 degrading peptide having future translational potential.
被引量：- 发表：2024
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NAPRT Silencing in FH-Deficient Renal Cell Carcinoma Confers Therapeutic Vulnerabilities via NAD+ Depletion.
被引量：- 发表：2024
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lncRNA-WAL promotes triple-negative breast cancer aggression by inducing β-catenin nuclear translocation.
Because of its insensitivity to existing radiotherapy, namely, chemotherapy and targeted treatments, triple-negative breast cancer (TNBC) remains a great challenge to overcome. Increasing evidence has indicated abnormal Wnt/β-catenin pathway activation in TNBC but not luminal or HER2+ breast cancer, and lncRNAs play a key role in a variety of cancers. Through lncRNA microarray profiling between activated and inactivated Wnt/β-catenin pathway of TNBC tissues, lnc-WAL (Wnt/β-catenin-associated lncRNA; WAL) was selected as the top upregulated lncRNA in Wnt/β-catenin pathway activation compared with the inactivation group. RNA immunoprecipitation sequencing was used to compare the β-catenin and IgG groups, in which lnc-WAL could interact with β-catenin. Clinically, increased lnc-WAL in TNBC tumor tissue was associated with shorter survival. lnc-WAL promoted epithelial-mesenchymal transition, the proliferation, migration, and invasion of breast cancer stem cells and TNBC cells. Mechanistically, lnc-WAL inhibited β-catenin protein degradation via AXIN-mediated phosphorylation at serine 45. Subsequently, β-catenin accumulated in the nucleus and activated the target genes. Importantly, Wnt/β-catenin pathway activation stimulated the transcription of lnc-WAL. These results pointed to a master regulatory role of lnc-WAL/AXIN/β-catenin in the malignant progression of TNBC. Our findings provide important clinical translational evidence that lnc-WAL may be a potential therapeutic target against TNBC. Implications: The positive feedback between lnc-WAL and the Wnt/β-catenin pathway promotes TNBC progression, and lnc-WAL could be a potential prognostic marker for patients with TNBC.
被引量：1 发表：1970
