Bortezomib inhibits gastric carcinoma HGC-27 cells through the phospho-Jun N-terminal kinase (p-JNK) pathway in vitro

Zhang, BeiLi; Gu, Yu

doi:10.1016/j.gene.2015.01.035

Cited by 3 publications

(3 citation statements)

References 29 publications

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“…More recently, the ability of bortezomib to downregulate the PI3K/AKT/mTOR pathway which is upstream of the HIF-1 pathway was demonstrated in prostate cancer cells 79 . Based on this discovery, recent studies were designed to assess the anticancer spectrum of bortezomib as sole agent or adjuvant therapy for the treatment of different types of cancers 80 , 81 , 82 .…”

Section: Molecules Intervening the Hif-1 α Pathwaymentioning

confidence: 99%

HIF-1α pathway: role, regulation and intervention for cancer therapy

Masoud

2015

Acta Pharmaceutica Sinica B

1,531

1,198

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Hypoxia-inducible factor-1 (HIF-1) has been recognized as an important cancer drug target. Many recent studies have provided convincing evidences of strong correlation between elevated levels of HIF-1 and tumor metastasis, angiogenesis, poor patient prognosis as well as tumor resistance therapy. It was found that hypoxia (low O2 levels) is a common character in many types of solid tumors. As an adaptive response to hypoxic stress, hypoxic tumor cells activate several survival pathways to carry out their essential biological processes in different ways compared with normal cells. Recent advances in cancer biology at the cellular and molecular levels highlighted the HIF-1α pathway as a crucial survival pathway for which novel strategies of cancer therapy could be developed. However, targeting the HIF-1α pathway has been a challenging but promising progresses have been made in the past twenty years. This review summarizes the role and regulation of the HIF-1α in cancer, and recent therapeutic approaches targeting this important pathway.

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Section: Molecules Intervening the Hif-1 α Pathwaymentioning

confidence: 99%

HIF-1α pathway: role, regulation and intervention for cancer therapy

Masoud

2015

Acta Pharmaceutica Sinica B

1,531

1,198

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“…Bortezomib was the first proteasome inhibitor approved by the US Food and Drug Administration in multiple myeloma (143). In vitro, bortezomib has a significant negative effect on the growth of GC cells (144). It is possible that bortezomib may become a common adjuvant therapeutic target in GC because it has a significant negative effect on the proliferation of GC cells (144).…”

Section: Therapeutics Targeting E3 Ligases In Gcmentioning

confidence: 99%

“…In vitro, bortezomib has a significant negative effect on the growth of GC cells (144). It is possible that bortezomib may become a common adjuvant therapeutic target in GC because it has a significant negative effect on the proliferation of GC cells (144). However, only a few E3 ligase-targeting molecules have the ability to suppress the progression of GC.…”

Section: Therapeutics Targeting E3 Ligases In Gcmentioning

confidence: 99%

Functional roles of E3 ubiquitin ligases in gastric cancer (Review)

Wang

Dai

et al. 2020

Oncol Lett

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To date, >650 E3 ubiquitin ligases have been described in humans, including >600 really interesting new genes (RINGs), 28 homologous to E6-associated protein C-terminus (HECTs) and several RING-in-between-RINGs. They are considered key regulators and therapeutic targets of many types of human cancers, including gastric cancer (GC). Among them, some RING and HECT E3 ligases are closely related to the proliferation, infiltration and prognosis of GC. During the past few years, abnormal expressions and functions of many E3 ligases have been identified in GC. However, the functional roles of E3 ligases in GC have not been fully elucidated. The present article focuses on the functional roles of E3 ligases related to the proteasome in GC. In this comprehensive review, the latest research progress on E3 ligases involved in GC and elaborate their structure, classification, functional roles and therapeutic value in GC was summarized. Finally, 30 E3 ligases that serve essential roles in regulating the development of GC were described. Some of these ligases may serve as oncogenes or tumor suppressors in GC, whereas the pathological mechanism of others needs further study; for example, constitutive photomorphogenic 1. In conclusion, the present review demonstrated that E3 ligases are crucial tumor regulatory factors and potential therapeutic targets in GC. Therefore, more studies should focus on the therapeutic targeting of E3 ligases in GC.

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