Silencing the<i>livin</i>gene enhances the cytotoxic effects of anticancer drugs on colon cancer cells

Oh, Bo Young; Kim, Kwang Ho; Chung, Sung-Chong; Lee, Ryung-Ah

doi:10.4174/astr.2016.91.6.273

Cited by 7 publications

(7 citation statements)

References 21 publications

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“…Therefore, in the present study, we investigated the role of Livin in determining susceptibility to commonly used chemotherapeutic drugs, such as docetaxel, cisplatin and 5-FU, in human HNSCC cell lines. Although several studies have described that Livin contribute to the resistance of various chemotherapeutic drugs including cisplatin in various cancers (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34), the present study is the first to demonstrate the correlation between Livin and chemoresistance in human HNSCC.…”

Section: Introductionmentioning

confidence: 81%

“…Wang et al (29) reported that shRNA-mediated silencing of Livin induces chemosensitivity to cisplatin and 5-FU in gastric cancer. Wang et al (30) and Oh et al (32) showed that Livin contributes to the resistance to 5-FU/vincristine/etoposide or 5-FU/leucovorin/oxaliplatin in colon cancer. Livin knockdown also increased chemosensitivity to adriamycin and cisplatin in non-small cell lung cancer (31).…”

Section: Discussionmentioning

confidence: 99%

“…Livin, a recently discovered IAP, is composed of a single BIR domain and a RING motif (9). Livin has been implicated in chemoresistance in various cancers (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34). It has been reported to play a role in resistance to cisplatin in bladder cancer, renal carcinoma, gastic cancer, hepatocellular carcinoma, lung adenocarcinoma/ non-small cell carcinoma, osteosarcoma, colon cancer and ovarian carcinoma (20)(21)(22)(23)(24)(25)(26)(27)(28)(29)31).…”

Section: Discussionmentioning

confidence: 99%

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Livin enhances chemoresistance in head and neck squamous cell carcinoma

et al. 2017

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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.

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Section: Introductionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Livin enhances chemoresistance in head and neck squamous cell carcinoma

et al. 2017

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“…Pharmacological advances targeting BIRC7 in cancer: Treatment with siRNA targeting BIRC7 significantly suppressed cancer cell growth and enhanced cytotoxicity of typical anticancer drugs such as 5-FU and oxaliplatin (L-OHP) in colorectal cancer, demonstrating such protein to be a relevant target in oncology (Oh et al, 2016). Similarly, a study using a protamine single-chain antibody fusion protein (anti-MM scFv-tP) to deliver BIRC7 siRNA to melanoma LiBr cells revealed suppression of cell proliferation and induction of apoptosis, both in vitro and in vivo (Wang et al, 2017).…”

Section: To Be Notedmentioning

confidence: 99%

BIRC7 (baculoviral IAP repeat containing 7)

Rigato¹,

Branco²,

Silva³

et al. 2020

Atlas of Genetics and Cytogenetics in Oncology and Haematology

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BIRC7, also known as livin, is a member of the Inhibitor of Apoptosis Protein (IAP) family and is linked to the prevention of cell death induced by apoptosis, by directly or indirectly preventing caspase activity. In general, as most IAPs, BIRC7 expression is not detectable in normal differentiated adult tissues, with the exception of placenta, spleen, lymph nodes and developing embryonic tissues. On the other hand, BIRC7 overexpression has been reported in a variety of tumor types, in which it is associated to malignancy and chemoresistance. Currently, there are some unanswered questions about BIRC7, including its interaction with caspases, a potential paradoxical role in the apoptotic process, and specific functions/affinities of the BIRC7α and BIRC7β splice variants. Moreover, several studies have demonstrated the value of BIRC7 as a therapeutic target in a number of cancer types. This review mainly focuses on the role of BIRC7 in cancer cell biology and its clinical significance, demonstrating aspects of its DNA/RNA and protein, as well as its relevance in cancer diagnosis and prognosis.

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“…In the study by Oh Y. B. et al [62] siRNA-mediated down-regulation of livin gene expression and it was observed that it could significantly suppress colon cancer growth and enhance the cytotoxic effects of the anticancer drugs 5-FU and L-OHP. It was observed that silencing livin gene expression in combination with treatment with anticancer drugs might be a novel dual anti-cancer therapy for CRC.…”

Section: Gene Therapymentioning

confidence: 99%

Colorectal Cancer from Molecular Pathways to Gene Therapy

Kosmıdis¹,

Efthimidis²,

Baka³

et al. 2017

Oncomedicine

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Nowadays colorectal cancer is still considered the third most common cancer in the world. The tumorigenesis mechanisms of colorectal cancer have been widely studied at a molecular level. It has been observed that morbidity and mortality caused by colorectal cancer impacts on the global economy. This occurs through the loss of productivity and the burden on the healthcare system. Therefore an effort is made by several researchers to expend considerably their resources to develop treatments and preventative strategies to reduce the incidence of colorectal cancer. A Large-scale sequencing of genome, proteome, microbiome, and transcriptome analyses of colorectal cancer tissue has allowed researchers to better understand colorectal cancer subtypes. Until now the following parameters have been identified with the etiology of colorectal cancer genetic mutations, inflammatory processes, diet, and the gut microbes. In the current review we will present the molecular pathways of CRC and discuss novel gene therapy approaches.

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Silencing thelivingene enhances the cytotoxic effects of anticancer drugs on colon cancer cells

Cited by 7 publications

References 21 publications

Livin enhances chemoresistance in head and neck squamous cell carcinoma

Livin enhances chemoresistance in head and neck squamous cell carcinoma

BIRC7 (baculoviral IAP repeat containing 7)

Colorectal Cancer from Molecular Pathways to Gene Therapy

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