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Role of JNK signaling in oral cancer: A mini review.

Abstract JNKs (c-Jun N-terminal kinases) belong to mitogen-activated protein kinases' family and become activated by several growth factors, stress, radiation, and other extracellular signals. In turn, JNK activation results in phosphorylation of downstream molecules involved in many normal cellular processes. Nevertheless, recent data have linked JNK signaling with several pathological conditions, including neurodegenerative diseases, inflammation, and cancer. The role of JNK in cancer remains controversial. Initially, JNK was thought to play a rather oncosuppressive role by mediating apoptosis in response to stress stimuli, inflammatory, or oncogenic signals. However, a number of studies have implicated JNK in malignant transformation and tumor growth. The contradictory functions of JNK in cancer may be due to the diversity of JNK upstream and downstream signaling and are under intensive investigation. This review summarizes current literature focusing on the significance of JNK pathway in cancer development and progression, particularly addressing its role in oral cancer. Understanding the complexity of JNK signaling has the potential to elucidate important molecular aspects of oral cancer, possibly leading to development of novel and individualized therapeutic strategies.
PMID
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Authors

Mayor MeshTerms
Keywords

JNK

apoptosis

oral cancer

signaling

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28639904
OWN - NLM
STAT- MEDLINE
DA  - 20170622
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Role of JNK signaling in oral cancer: A mini review.
PG  - 1010428317711659
LID - 10.1177/1010428317711659 [doi]
AB  - JNKs (c-Jun N-terminal kinases) belong to mitogen-activated protein kinases'
      family and become activated by several growth factors, stress, radiation, and
      other extracellular signals. In turn, JNK activation results in phosphorylation
      of downstream molecules involved in many normal cellular processes. Nevertheless,
      recent data have linked JNK signaling with several pathological conditions,
      including neurodegenerative diseases, inflammation, and cancer. The role of JNK
      in cancer remains controversial. Initially, JNK was thought to play a rather
      oncosuppressive role by mediating apoptosis in response to stress stimuli,
      inflammatory, or oncogenic signals. However, a number of studies have implicated 
      JNK in malignant transformation and tumor growth. The contradictory functions of 
      JNK in cancer may be due to the diversity of JNK upstream and downstream
      signaling and are under intensive investigation. This review summarizes current
      literature focusing on the significance of JNK pathway in cancer development and 
      progression, particularly addressing its role in oral cancer. Understanding the
      complexity of JNK signaling has the potential to elucidate important molecular
      aspects of oral cancer, possibly leading to development of novel and
      individualized therapeutic strategies.
FAU - Gkouveris, Ioannis
AU  - Gkouveris I
AD  - 1 Division of Diagnostic and Surgical Sciences, UCLA School of Dentistry, Los
      Angeles, CA, USA.
FAU - Nikitakis, Nikolaos G
AU  - Nikitakis NG
AD  - 2 Department of Oral Pathology and Medicine, Dental School, National and
      Kapodistrian University of Athens, Athens, Greece.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Apoptosis/genetics
MH  - Enzyme Activation/genetics
MH  - Humans
MH  - JNK Mitogen-Activated Protein Kinases/*genetics
MH  - MAP Kinase Signaling System/*genetics
MH  - Mouth Neoplasms/*genetics/pathology
MH  - Phosphorylation
MH  - Signal Transduction/genetics
OTO - NOTNLM
OT  - JNK
OT  - apoptosis
OT  - oral cancer
OT  - signaling
EDAT- 2017/06/24 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/23 06:00
AID - 10.1177/1010428317711659 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317711659. doi: 10.1177/1010428317711659.