Regulating Tumorigenicity and Cancer Metastasis through TRKA Signaling
Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net..
Tropomyosin receptor kinase (TRK) A, TRKA, is a specific binding receptor of nerve growth factor (NGF), which plays an essential role in the occurrence and progression of human cancers. TRKA overexpression has been proven to be a powerful carcinogenic driver and has been verified in many tumors. The TRKA receptor kinase domain is over-activated in an NGF-dependent manner, accompanied by activation of downstream signal pathways, such as RAS-MAPK, PI3K-AKT, JAK2-STAT3 pathway, PLC γ pathway, and Hippo pathway, which participate in tumor cell proliferation, invasion, epithelial-mesenchymal transition (EMT), perineural invasion (PNI), drug resistance, and cancer pain. In addition, chimeric oncogenes produced by the fusion of NTRK1 and other genes are also the direct cause of tumorigenesis and cancer development. The newly developed TRK inhibitors can improve symptoms and tumor regression in cancer patients with overexpression of TRKA or NTRK1 fusion gene. With the emergence of drug resistance, next generation of TRK inhibitors can still maintain strong clinical efficacy in the case of TRK kinase domain mutations, and these inhibitors are in clinical trials. This review summarizes the characteristics and research progress of TRKA, focusing on the regulatory role of the TRKA signal pathway in different tumors. In addition, we have summarized the clinical significance of TRKA and the TRK inhibitors. This review may provide a new reference for the study of the mechanism of TRKA in different tumors, and also provide a new perspective for the in-depth understanding of the role of TRKA as a biomarker and therapeutic target in human cancer.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2024 |
---|---|
Erschienen: |
2024 |
Enthalten in: |
Zur Gesamtaufnahme - volume:24 |
---|---|
Enthalten in: |
Current cancer drug targets - 24(2024), 3 vom: 05., Seite 271-287 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Fan, Yichao [VerfasserIn] |
---|
Links: |
---|
Anmerkungen: |
Date Completed 05.04.2024 Date Revised 05.04.2024 published: Print Citation Status MEDLINE |
---|
doi: |
10.2174/1568009623666230904150957 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM361683693 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | NLM361683693 | ||
003 | DE-627 | ||
005 | 20240405233116.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231226s2024 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.2174/1568009623666230904150957 |2 doi | |
028 | 5 | 2 | |a pubmed24n1366.xml |
035 | |a (DE-627)NLM361683693 | ||
035 | |a (NLM)37670705 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Fan, Yichao |e verfasserin |4 aut | |
245 | 1 | 0 | |a Regulating Tumorigenicity and Cancer Metastasis through TRKA Signaling |
264 | 1 | |c 2024 | |
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 05.04.2024 | ||
500 | |a Date Revised 05.04.2024 | ||
500 | |a published: Print | ||
500 | |a Citation Status MEDLINE | ||
520 | |a Copyright© Bentham Science Publishers; For any queries, please email at epubbenthamscience.net. | ||
520 | |a Tropomyosin receptor kinase (TRK) A, TRKA, is a specific binding receptor of nerve growth factor (NGF), which plays an essential role in the occurrence and progression of human cancers. TRKA overexpression has been proven to be a powerful carcinogenic driver and has been verified in many tumors. The TRKA receptor kinase domain is over-activated in an NGF-dependent manner, accompanied by activation of downstream signal pathways, such as RAS-MAPK, PI3K-AKT, JAK2-STAT3 pathway, PLC γ pathway, and Hippo pathway, which participate in tumor cell proliferation, invasion, epithelial-mesenchymal transition (EMT), perineural invasion (PNI), drug resistance, and cancer pain. In addition, chimeric oncogenes produced by the fusion of NTRK1 and other genes are also the direct cause of tumorigenesis and cancer development. The newly developed TRK inhibitors can improve symptoms and tumor regression in cancer patients with overexpression of TRKA or NTRK1 fusion gene. With the emergence of drug resistance, next generation of TRK inhibitors can still maintain strong clinical efficacy in the case of TRK kinase domain mutations, and these inhibitors are in clinical trials. This review summarizes the characteristics and research progress of TRKA, focusing on the regulatory role of the TRKA signal pathway in different tumors. In addition, we have summarized the clinical significance of TRKA and the TRK inhibitors. This review may provide a new reference for the study of the mechanism of TRKA in different tumors, and also provide a new perspective for the in-depth understanding of the role of TRKA as a biomarker and therapeutic target in human cancer | ||
650 | 4 | |a Review | |
650 | 4 | |a Journal Article | |
650 | 4 | |a TRKA | |
650 | 4 | |a TRKA fusion | |
650 | 4 | |a TRKA inhibitor | |
650 | 4 | |a TRKA overexpression | |
650 | 4 | |a targeted therapies | |
650 | 4 | |a tumorigenicity. | |
650 | 7 | |a Nerve Growth Factor |2 NLM | |
650 | 7 | |a 9061-61-4 |2 NLM | |
650 | 7 | |a Phosphatidylinositol 3-Kinases |2 NLM | |
650 | 7 | |a EC 2.7.1.- |2 NLM | |
650 | 7 | |a Receptor, trkA |2 NLM | |
650 | 7 | |a EC 2.7.10.1 |2 NLM | |
700 | 1 | |a Zhang, Boya |e verfasserin |4 aut | |
700 | 1 | |a Du, Xinhui |e verfasserin |4 aut | |
700 | 1 | |a Wang, Bangmin |e verfasserin |4 aut | |
700 | 1 | |a Yan, Qiang |e verfasserin |4 aut | |
700 | 1 | |a Guo, Liangyu |e verfasserin |4 aut | |
700 | 1 | |a Yao, Weitao |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t Current cancer drug targets |d 2001 |g 24(2024), 3 vom: 05., Seite 271-287 |w (DE-627)NLM120490560 |x 1873-5576 |7 nnns |
773 | 1 | 8 | |g volume:24 |g year:2024 |g number:3 |g day:05 |g pages:271-287 |
856 | 4 | 0 | |u http://dx.doi.org/10.2174/1568009623666230904150957 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 24 |j 2024 |e 3 |b 05 |h 271-287 |