A proteomic analysis of p53-independent induction of apoptosis by bortezomib in 4T1 breast cancer cell line

Yerlikaya, Azmi; Okur, Emrah; Baykal, Ahmet Tarık; Acılan, Ceyda; Boyacı, İhsan; Ulukaya, Engin

doi:10.1016/j.jprot.2014.09.010

Cited by 25 publications

(16 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…PSMD14 is a deubiquitinating enzyme responsible for substrate deubiquitination during proteasomal degradation. Although the role of PSMD14 has been reported in several cancer types [17,19,21,22,25,34], its involvement in lung cancer has not been elucidated. In this study, we found that the level of PSMD14 was significantly upregulated in NSCLC tissues, suggesting its tumor-promoting effects in NSCLC.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of deubiquitinase PSMD14 in lung adenocarcinoma (LUAD) and its prognostic significance

Zhang¹,

Xu²,

Ma³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

PSMD14 is a 19S-proteasome-associated deubiquitinating enzyme that facilitates protein degradation by the 20S proteasome core particle. Although accumulating evidence indicates that PSMD14 has emerged as a critical oncogenic factor by promoting tumor growth, the expression and function of PSMD14 in non-small cell lung cancer (NSCLC) remain largely unknown. In this study, we assessed PSMD14 expression and correlated it with clinical-pathological features and patient survival in NSCLC. We also determined the roles of PSMD14 in the regulation of lung adenocarcinoma (LUAD) cell growth. The results showed that PSMD14 expression was significantly upregulated in human NSCLC tissues compared with adjacent non-cancerous tissues. The PSMD14 level was associated with tumor size, lymph node invasion, and TNM stage in LUAD patients. Importantly, high PSMD14 expression was associated with poor overall survival (OS) and disease-free survival (DFS) in LUAD patients. Further, knockdown of PSMD14 significantly inhibited cell growth and caused G1 arrest and cellular senescence by increasing p21 stability in LUAD cells. PSMD14 knockdown also promoted cell apoptosis by increasing cleaved caspase-3 levels in H1299 cells. PSMD14 may serve as a potential prognostic marker and therapeutic target for LUAD patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Upregulation of deubiquitinase PSMD14 in lung adenocarcinoma (LUAD) and its prognostic significance

Zhang¹,

Xu²,

Ma³

et al. 2020

J. Cancer

View full text Add to dashboard Cite

show abstract

“…LL-37 in gastric cancer cells acts as cancer-suppressing agent due to its ability to inhibit the proteasome in gastric tumor tissues (Wu et al 2010b ). The proteasome is the main system linked with intracellular protein degradation and its connection with cell proliferation, apoptosis, and stabilization of cell cycle has made it an attractive target for cancer therapy (Krętowski et al 2015 ; Richardson et al 2005 ; Steg et al 2014 ; Wu et al 2010a ; Yerlikaya et al 2015 ). In gastric cancer cells, human cathelicidin inhibited the proteasome, promoting signaling through the bone morphogenic protein (BMP) pathway.…”

Section: Gastric Cancermentioning

confidence: 99%

The Role of Cathelicidin LL-37 in Cancer Development

Piktel

Niemirowicz

Wnorowska

et al. 2015

Arch. Immunol. Ther. Exp.

View full text Add to dashboard Cite

LL-37 is a C-terminal peptide proteolytically released from 18 kDa human cathelicidin protein (hCAP18). Chronic infections, inflammation, tissue injury and tissue regeneration are all linked with neoplastic growth, and involve LL-37 antibacterial and immunomodulatory functions. Such a link points to the possible involvement of LL-37 peptide in carcinogenesis. An increasing amount of evidence suggests that LL-37 can have two different and contradictory effects—promotion or inhibition of tumor growth. The mechanisms are tissue-specific, complex, and depend mostly on the ability of LL-37 to act as a ligand for different membrane receptors whose expression varies on different cancer cells. Overexpression of LL-37 was found to promote development and progression of ovarian, lung and breast cancers, and to suppress tumorigenesis in colon and gastric cancer. This review explores and summarizes the current views on how LL-37 contributes to immunity, pathophysiology and cell signaling involved in malignant tumor growth.

show abstract

“…4T1 is a p53-deficient breast cancer cell line (35,36). Triple-negative breast cancer cell lines [i.e., lacking the estrogen receptor (ER), progesterone receptor, and human epidermal growth factor receptor 2 (HER2)] are less affected by estrogen than traditional cell lines (37,38).…”

Section: Introductionmentioning

confidence: 99%

Aspirin and metformin exhibit antitumor activity in murine breast cancer

Zhao

Wang

et al. 2018

Oncol Rep

View full text Add to dashboard Cite

Abstract. Studies have shown that aspirin and metformin play important roles in chemoprevention and repression of breast cancers, even though the exact mechanism remains unclear. Aspirin is capable of stimulating apoptosis through prostaglandin-dependent or prostaglandin-independent pathways. Metformin inhibits cell growth by enhancing the tumor suppressive function of transforming growth factor (TGF-β).In the present study, we report a new link between aspirin, metformin, TGF-β1 and murine breast cancer inhibition. Specifically, we showed that aspirin and metformin enhanced 4T1 cell apoptosis by inducing secretion of TGF-β1, whereas estradiol weakened the effect.

show abstract

A proteomic analysis of p53-independent induction of apoptosis by bortezomib in 4T1 breast cancer cell line

Cited by 25 publications

References 41 publications

Upregulation of deubiquitinase PSMD14 in lung adenocarcinoma (LUAD) and its prognostic significance

Upregulation of deubiquitinase PSMD14 in lung adenocarcinoma (LUAD) and its prognostic significance

The Role of Cathelicidin LL-37 in Cancer Development

Aspirin and metformin exhibit antitumor activity in murine breast cancer

Contact Info

Product

Resources

About