BDNF and its signaling in cancer
© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature..
PURPOSE: Brain-derived neurotrophic factor (BDNF) belongs to the family of neurotrophic factors that can potentially increase cancer cell growth, survival, proliferation, anoikis, and migration by tyrosine kinase receptors TrkB and the p75NTR death receptor. The activation of BDNF/TrkB pathways leads to several downstream signaling pathways, including PI3K/Akt, Jak/STAT, PLCγ, Ras-Raf-MEK-ERK, NF-kB, and transactivation of EGFR. The current review aimed to provide an overview of the role of BDNF and its signaling in cancer.
METHODS: We searched a major medical database, PubMed, to identify eligible studies for a narrative synthesis.
RESULTS: Pathological examinations demonstrate BDNF overexpression in human cancer, notably involving the prostate, lung, breast, and underlying tissues, associated with a higher death rate and poor prognosis. Therefore, measurement of BDNF, either for identifying the disease or predicting response to therapy, can be helpful in cancer patients. Expression profiling studies have recognized the role of microRNAs (miR) in modulating BDNF/TrkB pathways, such as miR-101, miR-107, miR-134, miR-147, miR-191, miR-200a/c, miR-204, miR-206, miR-210, miR-214, miR-382, miR-496, miR-497, miR-744, and miR-10a-5p, providing a potential biological mechanism by which targeted therapies may correlate with decreased BDNF expression in cancers. Clinical studies investigating the use of agents targeting BDNF receptors and related signaling pathways and interfering with the related oncogenic effect, including Entrectinib, Larotrectinib, Cabozantinib, Repotrectinib, Lestaurtinib, and Selitrectinib, are in progress.
CONCLUSION: The aberrant signaling of BDNF is implicated in various cancers. Well-designed clinical trials are needed to clarify the BDNF role in cancer progression and target it as a therapeutic method.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2023 |
---|---|
Erschienen: |
2023 |
Enthalten in: |
Zur Gesamtaufnahme - volume:149 |
---|---|
Enthalten in: |
Journal of cancer research and clinical oncology - 149(2023), 6 vom: 01. Juni, Seite 2621-2636 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Malekan, Mohammad [VerfasserIn] |
---|
Links: |
---|
Anmerkungen: |
Date Completed 27.04.2023 Date Revised 27.04.2023 published: Print-Electronic Citation Status MEDLINE |
---|
doi: |
10.1007/s00432-022-04365-8 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM346890179 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM346890179 | ||
003 | DE-627 | ||
005 | 20231226032529.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231226s2023 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1007/s00432-022-04365-8 |2 doi | |
028 | 5 | 2 | |a pubmed24n1156.xml |
035 | |a (DE-627)NLM346890179 | ||
035 | |a (NLM)36173463 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Malekan, Mohammad |e verfasserin |4 aut | |
245 | 1 | 0 | |a BDNF and its signaling in cancer |
264 | 1 | |c 2023 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 27.04.2023 | ||
500 | |a Date Revised 27.04.2023 | ||
500 | |a published: Print-Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a © 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature. | ||
520 | |a PURPOSE: Brain-derived neurotrophic factor (BDNF) belongs to the family of neurotrophic factors that can potentially increase cancer cell growth, survival, proliferation, anoikis, and migration by tyrosine kinase receptors TrkB and the p75NTR death receptor. The activation of BDNF/TrkB pathways leads to several downstream signaling pathways, including PI3K/Akt, Jak/STAT, PLCγ, Ras-Raf-MEK-ERK, NF-kB, and transactivation of EGFR. The current review aimed to provide an overview of the role of BDNF and its signaling in cancer | ||
520 | |a METHODS: We searched a major medical database, PubMed, to identify eligible studies for a narrative synthesis | ||
520 | |a RESULTS: Pathological examinations demonstrate BDNF overexpression in human cancer, notably involving the prostate, lung, breast, and underlying tissues, associated with a higher death rate and poor prognosis. Therefore, measurement of BDNF, either for identifying the disease or predicting response to therapy, can be helpful in cancer patients. Expression profiling studies have recognized the role of microRNAs (miR) in modulating BDNF/TrkB pathways, such as miR-101, miR-107, miR-134, miR-147, miR-191, miR-200a/c, miR-204, miR-206, miR-210, miR-214, miR-382, miR-496, miR-497, miR-744, and miR-10a-5p, providing a potential biological mechanism by which targeted therapies may correlate with decreased BDNF expression in cancers. Clinical studies investigating the use of agents targeting BDNF receptors and related signaling pathways and interfering with the related oncogenic effect, including Entrectinib, Larotrectinib, Cabozantinib, Repotrectinib, Lestaurtinib, and Selitrectinib, are in progress | ||
520 | |a CONCLUSION: The aberrant signaling of BDNF is implicated in various cancers. Well-designed clinical trials are needed to clarify the BDNF role in cancer progression and target it as a therapeutic method | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Review | |
650 | 4 | |a BDNF | |
650 | 4 | |a Biomarker | |
650 | 4 | |a Cancer | |
650 | 4 | |a Pan-Trk inhibitors | |
650 | 4 | |a Therapeutic targeting | |
650 | 4 | |a TrkB | |
650 | 4 | |a microRNA | |
650 | 7 | |a Brain-Derived Neurotrophic Factor |2 NLM | |
650 | 7 | |a Phosphatidylinositol 3-Kinases |2 NLM | |
650 | 7 | |a EC 2.7.1.- |2 NLM | |
650 | 7 | |a MicroRNAs |2 NLM | |
650 | 7 | |a MIRN204 microRNA, human |2 NLM | |
650 | 7 | |a MIRN206 microRNA, human |2 NLM | |
650 | 7 | |a MIRN214 microRNA, human |2 NLM | |
650 | 7 | |a MIRN496 microRNA, human |2 NLM | |
650 | 7 | |a MIRN497 microRNA, human |2 NLM | |
700 | 1 | |a Nezamabadi, Sasan Salehi |e verfasserin |4 aut | |
700 | 1 | |a Samami, Elham |e verfasserin |4 aut | |
700 | 1 | |a Mohebalizadeh, Mehdi |e verfasserin |4 aut | |
700 | 1 | |a Saghazadeh, Amene |e verfasserin |4 aut | |
700 | 1 | |a Rezaei, Nima |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Journal of cancer research and clinical oncology |d 1981 |g 149(2023), 6 vom: 01. Juni, Seite 2621-2636 |w (DE-627)NLM000394610 |x 1432-1335 |7 nnns |
773 | 1 | 8 | |g volume:149 |g year:2023 |g number:6 |g day:01 |g month:06 |g pages:2621-2636 |
856 | 4 | 0 | |u http://dx.doi.org/10.1007/s00432-022-04365-8 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 149 |j 2023 |e 6 |b 01 |c 06 |h 2621-2636 |