Tropomyosin receptor kinase B (<scp>TrkB</scp>) signalling: targeted therapy in neurogenic tumours

Li, Yuehua; Wei, Cheng-Jiang; Wang, Wei; Li, Qingfeng; Wang, Zhichao

doi:10.1002/cjp2.307

Cited by 6 publications

(6 citation statements)

References 109 publications

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“…These pathways consequently support gene transcription, cell growth, and survival. The most frequent fusions discovered involved the NTRK gene, with others concerning the BRAF, rearrangement during transfection (RET), FGFR, ROS Proto‐Oncogene 1 Receptor Tyrosine Kinase 1 (ROS1), and anaplastic lymphoma kinase (ALK) genes 111,112 . In tumors with high MSI scores and RAS/BRAF wild‐type levels, gene fusion rates were higher.…”

Section: Tissue‐based Biomarkersmentioning

confidence: 99%

“…109,110 Receptor Tyrosine Kinase 1 (ROS1), and anaplastic lymphoma kinase (ALK) genes. 111,112 In tumors with high MSI scores and RAS/BRAF wildtype levels, gene fusion rates were higher. Clinical characteristics of patients with these gene fusions included advanced age, right-sided primary tumors, higher lymphatic spread rates, and lower liver metastasis rates.…”

Section: Hepatocyte Growth Factor (Hgf) and C-metmentioning

confidence: 99%

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A perspective on emerging therapies in metastatic colorectal cancer: Focusing on molecular medicine and drug resistance

Kusumaningrum,

Makaba,

Ali

et al. 2024

Cell Biochemistry & Function

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The majority of cancer cases are colorectal cancer, which is also the second largest cause of cancer‐related deaths worldwide. Metastasis is the leading cause of death for patients with colorectal cancer. Metastatic colorectal cancer incidence are on the rise due to a tiny percentage of tumors developing resistant to medicines despite advances in treatment tactics. Cutting‐edge targeted medications are now the go‐to option for customized and all‐encompassing CRC care. Specifically, multitarget kinase inhibitors, antivascular endothelial growth factors, and epidermal growth factor receptors are widely used in clinical practice for CRC‐targeted treatments. Rare targets in metastatic colorectal cancer are becoming more well‐known due to developments in precision diagnostics and the extensive use of second‐generation sequencing technology. These targets include the KRAS mutation, the BRAF V600E mutation, the HER2 overexpression/amplification, and the MSI‐H/dMMR. Incorporating certain medications into clinical trials has significantly increased patient survival rates, opening new avenues and bringing fresh viewpoints for treating metastatic colorectal cancer. These focused therapies change how cancer is treated, giving patients new hope and better results. These markers can significantly transform and individualize therapy regimens. They could open the door to precisely customized and more effective medicines, improving patient outcomes and quality of life. The fast‐growing body of knowledge regarding the molecular biology of colorectal cancer and the latest developments in gene sequencing and molecular diagnostics are directly responsible for this advancement.

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Section: Tissue‐based Biomarkersmentioning

confidence: 99%

Section: Hepatocyte Growth Factor (Hgf) and C-metmentioning

confidence: 99%

A perspective on emerging therapies in metastatic colorectal cancer: Focusing on molecular medicine and drug resistance

Kusumaningrum,

Makaba,

Ali

et al. 2024

Cell Biochemistry & Function

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“…Great part of research identifying BDNF-target microRNAs regard to investigations on the oncogenicity of BDNF/TrkB signal transduction in tumor cell growth and metastasis (Y. Li et al, 2023;Ni & Zhang, 2020). A list of microRNAs found to degrade BDNF mRNA transcripts in oncology research follows: miR-10a, miR-22, miR-204, miR-107, miR-382, miR-496, miR-497, miR-584, miR-744, miR-26a-1 and miR-26a-2 subtypes (Caputo et al, 2011;Cheng et al, 2018;B.…”

Section: Bdnf By Micrornasmentioning

confidence: 99%

BDNF Modulation by microRNAs: An Update on the Experimental Evidence

de Assis,

Murawska-cialowicz

2024

Preprint

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MicroRNAs can interfere with a protein function by suppressing their messenger RNA translation or the synthesis of its related factors. The function of brain-derived neurotrophic factor (BDNF) is essential to the proper formation and function of the nervous system and is seen to be regulated by many microRNAs. However, understanding how microRNAs influence BDNF actions within cells requires a wider comprehension of their integrative regulatory mechanisms. Aim: In this literature review, we have synthesized the evidence of microRNA regulation on BDNF in cells and tissues, and provided an analytical discussion about direct and indirect mechanisms that appeared involved in BDNF regulation by microRNAs. Methods: Searches were conducted on PubMed.gov using the terms “BDNF” AND “MicroRNA” and “brain-derived neurotrophic factor” AND “MicroRNA”, updated on September 1st, 2023. Papers without open access were requested from the authors. One hundred and seventy-one papers were included for review and discussion. Results and Discussion: The local regulation of BDNF by microRNAs involves a complex interaction between a series of microRNAs with target proteins that can either inhibit or enhance BDNF expression, at the core of cell metabolism. Therefore, understanding this homeostatic balance provides resources for the future development of vector-delivery-based therapies for the neuroprotective effects of BDNF.

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“…TrkB is a significant suppression target in many cancer cells [ 92 – 95 ], as in many other conditions driven by excessive proliferation, such as endometriosis [ 96 ]. TrkB activation enhances the survival and proliferation of cancer stem-like cells as well as increasing metastasis, epithelial-mesenchymal transition (EMT), vascular invasion and poor prognosis [ 97 – 100 ].…”

Section: Cortisol Melatonin Trkb and Tumor Microenvironment Cellsmentioning

confidence: 99%

Melatonin, BAG-1 and cortisol circadian interactions in tumor pathogenesis and patterned immune responses

Anderson

2023

Exploration of Targeted Anti-Tumor Therapy

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A dysregulated circadian rhythm is significantly associated with cancer risk, as is aging. Both aging and circadian dysregulation show suppressed pineal melatonin, which is indicated in many studies to be linked to cancer risk and progression. Another independently investigated aspect of the circadian rhythm is the cortisol awakening response (CAR), which is linked to stress-associated hypothalamus-pituitary-adrenal (HPA) axis activation. CAR and HPA axis activity are primarily mediated via activation of the glucocorticoid receptor (GR), which drives patterned gene expression via binding to the promotors of glucocorticoid response element (GRE)-expressing genes. Recent data shows that the GR can be prevented from nuclear translocation by the B cell lymphoma-2 (Bcl-2)-associated athanogene 1 (BAG-1), which translocates the GR to mitochondria, where it can have diverse effects. Melatonin also suppresses GR nuclear translocation by maintaining the GR in a complex with heat shock protein 90 (Hsp90). Melatonin, directly and/or epigenetically, can upregulate BAG-1, suggesting that the dramatic 10-fold decrease in pineal melatonin from adolescence to the ninth decade of life will attenuate the capacity of night-time melatonin to modulate the effects of the early morning CAR. The interactions of pineal melatonin/BAG-1/Hsp90 with the CAR are proposed to underpin how aging and circadian dysregulation are associated with cancer risk. This may be mediated via differential effects of melatonin/BAG-1/Hsp90/GR in different cells of microenvironments across the body, from which tumors emerge. This provides a model of cancer pathogenesis that better integrates previously disparate bodies of data, including how immune cells are regulated by cancer cells in the tumor microenvironment, at least partly via the cancer cell regulation of the tryptophan-melatonin pathway. This has a number of future research and treatment implications.

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Tropomyosin receptor kinase B (TrkB) signalling: targeted therapy in neurogenic tumours

Cited by 6 publications

References 109 publications

A perspective on emerging therapies in metastatic colorectal cancer: Focusing on molecular medicine and drug resistance

A perspective on emerging therapies in metastatic colorectal cancer: Focusing on molecular medicine and drug resistance

BDNF Modulation by microRNAs: An Update on the Experimental Evidence

Melatonin, BAG-1 and cortisol circadian interactions in tumor pathogenesis and patterned immune responses

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