Expression of IAP family proteins in colon cancers from patients with different age groups

Endo, Takashi; Abe, Shinya; Seidlar, Heinrich; Nagaoka, Sakae; Takemura, Tamiko; Utsuyama, Masanori; Kitagawa, Masanobu; Hirokawa, Katsuíku

doi:10.1007/s00262-004-0534-8

Cited by 59 publications

(49 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Chemoresistance results from a variety of complicated factors, including mutations in specific drug targets, impaired drug transporters, DNA repair activation, increased drug efflux and evasion of apoptosis by cancer cells (37,38). Among these mechanisms, evasion of apoptosis is considered a major cause of drug resistance since many chemotherapeutic agents act through the induction of apoptosis (6).…”

Section: Discussionmentioning

confidence: 99%

Livin enhances chemoresistance in head and neck squamous cell carcinoma

et al. 2017

View full text Add to dashboard Cite

Abstract. The responsiveness of head and neck squamous cell carcinoma (HNSCC) to chemotherapy widely affects prognosis. Overcoming chemoresistance is necessary to improve prognoses in patients with advanced HNSCC. Evasion of apoptosis by cancer cells is a major cause of chemoresistance. Livin, a member of the human inhibitors of apoptosis protein family, is highly expressed in various human cancer tissues and is associated with tumor progression and poor prognosis in human cancers. The aim of the present study was to evaluate the role of Livin in the susceptibility to popularly used chemotherapeutic drugs such as cisplatin, 5-fluorouracil (FU) and docetaxel in human HNSCC cell lines (SNU1041, PCI1 and PCI50 cells). Reverse transcription polymerase chain reaction and western blotting were performed to determine mRNA and protein expression levels. Cell viability and apoptosis assays were used to assess the functional effects of small-interfering RNA-mediated knockdown of Livin. Each HNSCC cell line had different sensitivity to chemotherapeutic drugs. Livin knockdown significantly enhanced cytotoxicity to cisplatin, 5-FU and docetaxel in human HNSCC cells. Livin knockdown induced apoptosis and enhanced chemotherapyinduced apoptosis to cisplatin, 5-FU and docetaxel. Consistent with this, Livin-knockdown cells showed greater expression of cleaved caspases-3 and -7 and poly(ADP-ribose)polymerase compared with that in control cells after cisplatin, 5-FU, or docetaxel treatment. In conclusion, our results suggest that siRNA-mediated Livin knockdown enhanced the chemosensitivity of the three HNSCC cell lines to cisplatin, 5-FU and docetaxel. Although further investigations are required to support these findings, our results demonstrated that novel therapeutic strategies with combined use of siRNA targeting Livin and chemotherapeutic agents may have applications in the treatment of advanced HNSCC.

show abstract

Section: Discussionmentioning

confidence: 99%

Livin enhances chemoresistance in head and neck squamous cell carcinoma

et al. 2017

View full text Add to dashboard Cite

show abstract

“…A previous study (Endo et al, 2004) found that NAIP mRNA expression was decreased in well and moderately differentiated colon adenocarcinoma, compared with adjacent BM-derived macrophage culture BM was flushed from the tibia and femur, red blood cells were lysed, and cells were cultured in BMDM medium (DMEM, 10% FCS, 20% supernatant from L929 cell-conditioned medium, 1% Penicillin-Streptomycin (10 000 U/ml; Invitrogen) in 10 cm culture Petri dishes for 6-7 d. Adherent cells were lifted from the Petri dish using Accutase (Invitrogen).…”

Section: Models Of Crc and Colitismentioning

confidence: 91%

Epithelial NAIPs protect against colonic tumorigenesis

Allam¹,

Maillard²,

Tardivel³

et al. 2015

J Cell Biol

View full text Add to dashboard Cite

“…Subsequently, it induces DNA damage recognition proteins to signal to downstream effectors such as p53, resulting in cell cycle arrest and apoptosis. To date, little is know on the Livin expression profile in CRC except for preliminary reports [17][18][19][20][21]. Neither is it known about the relationship between Livin expression and cisplatin sensitivity in CRC.…”

Section: Introductionmentioning

confidence: 99%

“…Several reports helped to expand its expression profile to variant tumors such as melanoma, leukemias, bladder, breast, cervical, nasopharyngeal and lung cancer [5][6][7][8]. However, there are only limited reports regarding its expression in CRC except some preliminary studies [17][18][19][20][21]. Previously, Livin expression was described in only 3 colon cancer cell lines (LoVo, Previous reports demonstrated that Livin contributed to resistance to fluorouracil, etoposide, and vincristine for tumor cells, but no studies were intended to explore the relationship between Livin expression and resistance to platinum.…”

mentioning

confidence: 99%

Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells

Ding

Liu

Olsson³

et al. 2012

Tumor Biol.

View full text Add to dashboard Cite

The anti-apoptotic factor Livin has been considered critical for tumor progression and poor prognosis for variant types of tumors. But there are only limited reports regarding its expression and biological functions in colon cancer. Here we examined Livin expression in four colon cancer cell lines (HCT116, RKO, KM12C and SW620) in the presence or absence of cisplatin which was used as a model reagent. We found the different response to cisplatin was related to endogenous Livin expression level. From among a panel of apoptosis-related factors (p53, Bcl-2, Bcl-XL, BAX, and survivin), the expression of Livin was up-regulated after cisplatin treatment in a dose-dependent manner. Both the immunocytochemistry and nuclear cytoplasmic fractionation indicated Livin remained in the cytoplasm after treatment with cisplatin. In an attempt to explore the mechanism, we found the elevated expression of Livin was not due to the decreased degradation by proteosome but was enhanced at the mRNA level. Besides, cisplatin treatment activated the mammalian target of rapamycin (mTOR) pathway as shown by increased phosphorylation of Akt1, mTOR, S6K, and 4E-BP1, together with the elevated Livin. The PI3K inhibitor LY294002 inhibited both the phosphorylation of mTOR and up-regulation of Livin. The stable over-expression of Livin inhibited the activation of caspase-3 and led to resistance to cisplatin, while the knock-down of Livin by siRNA rendered colon cancer cells more sensitive to cisplatin. Our study along with others highlighted the potential of Livin for cancer therapy in colon cancer.

show abstract

Expression of IAP family proteins in colon cancers from patients with different age groups

Cited by 59 publications

References 21 publications

Livin enhances chemoresistance in head and neck squamous cell carcinoma

Livin enhances chemoresistance in head and neck squamous cell carcinoma

Epithelial NAIPs protect against colonic tumorigenesis

Upregulation of the antiapoptotic factor Livin contributes to cisplatin resistance in colon cancer cells

Contact Info

Product

Resources

About