The BH3-only protein, PUMA, is involved in oxaliplatin-induced apoptosis in colon cancer cells

Wang, Xinying; Li, Ming; Wang, Jide; Yeung, Chung Man; Zhang, Hongquan; Kung, Hsiang Fu; Jiang, Bo; Lin, Marie Chia‐mi

doi:10.1016/j.bcp.2006.02.011

Cited by 41 publications

(36 citation statements)

References 33 publications

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“…However, an increasing number of studies have found that PUMA can be out of the p53-dependent status. Without considering the state of p53, PUMA adenovirus increases the sensitivity of esophageal cancer cells to anticancer drugs (40). Bryostatin 5 significantly increased the expression of PUMA but slightly increased p53 expression in acute monocytic leukemia cells (41).…”

Section: Discussionmentioning

confidence: 99%

Taurine induces the apoptosis of breast cancer cells by regulating apoptosis-related proteins of mitochondria

Zhang

Lü

Wang

et al. 2014

International Journal of Molecular Medicine

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Abstract. Taurine (Tau), the most abundant free amino acid in humans has numerous potential health benefits through its antioxidant and anti-inflammatory properties. However, limited studies have assessed its effect on tumors and the antitumor mechanism remains unknown. The present study investigated the cellular and molecular changes induced by Tau, leading to the induction of apoptosis in human breast cancer cell lines MCF-7 and MDA-MB-231. MCF-7 is p53 proficient (p53 +/+ ) and MDA-MB-231 is a p53 null mutant (p53 -/-). Cell proliferation and viability were assessed by MTT. Flow cytometry and hoechst33342 fluorescent staining were employed to detect apoptosis. Spectrophotometry was used to detect caspase-3 activity. Reverse transcription-polymerase chain reaction and western blot analysis were used to detect the levels of mRNA and proteins of p53-upregulated modulator of apoptosis (PUMA), Bax and Bcl-2. Finally, the affect of Tau on the growth of MDA-MB-231-cell-nude mice xenografts was examined. In the study, Tau inhibited growth and induced apoptosis of the two cell lines in a concentration-and time-dependent manner. Notably, the inhibitory effect of Tau on p53 -/-cancer cells was clearly significant compared to the p53 +/+ cancer cells. Further studies showed that Tau promoted apoptosis in human breast cancer cells and inhibited the growth of tumor in nude mice by inducing the expression of PUMA, which further up-and downregulated the expression of Bax and Bcl-2 protein, giving rise to increased activation of caspase-3. Collectively, these results indicate that Tau is a potent candidate for the chemotherapy of breast cancer through increasing the PUMA expression independent of p53 status. IntroductionIn recent years, cancer has become the leading cause of mortality, and it is detrimental to health and quality of life. Environmental chemical carcinogens have been estimated to contribute significantly to the causation of a sizable fraction, perhaps a majority, of human cancers, when exposures are correlated to 'life-style' factors, such as diet (1). Therefore, the anticancer substances in the diet have become of current interest in research for cancer prevention.Tau, chemically identified as 2-aminoethanesulfonic acid, is a sulfur-containing amino acid of a simple chemical structure. Tau accounts for ~0.1% of total human body weight and exists in a free-state in all the organs. However, the ability of endogenous Tau synthesis is limited. A large number of studies and clinical applications demonstrated that Tau has extensive physiological effects, and has been identified to be the endogenous anti-injury material. Recently, Tau has been used to in the therapy of diseases, including liver and gallbladder disease (2), cardiovascular disease (3), diabetes (4,5) and cataract (6,7). However, studies on its effect on tumors remains limited and the mechanism of its antitumor ability is ambiguous. Tau has been reported to protect cells from oxidant-induced injury by scavenging strong oxidant and cytotoxic agents (8). ...

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Section: Discussionmentioning

confidence: 99%

Taurine induces the apoptosis of breast cancer cells by regulating apoptosis-related proteins of mitochondria

Zhang

Lü

Wang

et al. 2014

International Journal of Molecular Medicine

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“…The human MnSOD expression plasmid was a gift from Dr Abbadie at the Institute of Biology of Lille, France (Bernard et al, 2001). Dominant-negative mutants of human MEK1 (DN-MEK1; Wang et al, 2006) and caspase-9 (Mashima et al, 2005) were described elsewhere.…”

Section: Antibodies and Reagentsmentioning

confidence: 99%

Chemosensitisation by manganese superoxide dismutase inhibition is caspase-9 dependent and involves extracellular signal-regulated kinase 1/2

et al. 2008

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Chemoresistance and therapeutic selectivity are major obstacles to successful chemotherapy of ovarian cancer. Manganese superoxide disumutase (MnSOD) is an important antioxidant enzyme responsible for the elimination of superoxide radicals. We reported here that MnSOD was significantly elevated in ovarian cancer cells and its overexpression was one of the mechanisms that increased resistance to apoptosis in cancer cells. Knockdown of MnSOD by small-interfering RNA (siRNA) led to an increase in superoxide generation and sensitisation of ovarian cancer cells to the two front-line anti-cancer agents doxorubicin and paclitaxel whose action involved free-radical generation. This synergistic effect was not observed in non-transformed ovarian surface epithelial cells. Furthermore, our results revealed that this combination at the cellular level augmented activation of caspase-3 and caspase-9, but not caspase-8, suggesting involvement of an intrinsic apoptotic pathway. Evaluation of signalling pathways showed that MnSOD siRNA enhanced doxorubicin-and paclitaxel-induced phosphorylation of extracellular signal-regulated kinase 1/2. Akt activation was not affected. These results identify a novel chemoresistance mechanism in ovarian cancer, and show that combination of drugs capable of suppressing MnSOD with conventional chemotherapeutic agents may provide a novel strategy with a superior therapeutic index and advantage for the treatment of refractory ovarian cancer.

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“…Western blotting analysis was assessed according to the protocol described before [23] . In brief, cells were washed with ice-cold PBS twice and lysed with ice-cold lysis buffer.…”

Section: Western Blotting Analysismentioning

confidence: 99%

Establishment and characterization of a new cell line derived from human colorectal laterally spreading tumor

Wang¹,

Lai²,

Yeung³

et al. 2008

WJG

Self Cite

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CONCLUSION:We established and characterized a colorectal cancer cell line, LST-R1 and LST-R1 has an obvious malignant tendency, which maybe partially attributed to the changes of the expression of some adhesion molecules, such as E-cadherin. It is also a versatile tool for exploring the original and progressive mechanisms of laterally spreading tumor and the early colon cancer genesis. INTRODUCTIONTwo routes have been described that can lead to colon carcinogenesis: one is the adenoma-carcinoma model, which is the main carcinogenetic pathway of prudent colorectal tumor and has been widely accepted in the west. However, an increasing number of superficial or flat colorectal tumors have been reported, particular in Japan [1,2] . The superficial tumors are considered to have a distinct clinicopathologic, genetic feature and behave a different carcinogenetic pathway, called de novo pathway [3][4][5][6] . Laterally spreading tumor (LST) is a unique subtype of superficial colorectal tumor, which was first reported by Kudo S in 1993 [7,8] and many names such as granular cluster type, nodule-aggregating tumor, creeping tumor, superficial spreading (epithelial) tumor, flower-bed-like lesion had been used. In 1998, it was defined as tumors originated from the colorectal mucous membranes and mainly extends laterally rather than vertically with its diameter greater than 1 cm ( Figure 1A) [9][10][11][12] . It has a tendency to affect the rectum, sigmoid colon, and caecum. In some studies, it has been reported that the carcinogenesis rate of LST is 8.64%-52.5% [13][14][15] . Abstract AIM: To study the molecular mechanism of laterally spreading tumor (LST), a cell line [Laterally Spreading Tumor-Rectum 1 (LST-R1)] was derived and the characteristics of this cell line were investigated. BASIC RESEARCH METHODS:A new cell line (LST-R1) originated from laterally spreading tumor was established. Properties of the cell line were characterized using scanning and transmission electron microscopy, immunohistochemistry method, cytogenetic analysis and nude mice xenograft experiments. In vitro invasion assay, cDNA microarray and Western blotting were used to compare the difference between the LST-R1 and other colorectal cancer cell lines derived from prudent colon cancer. RESULTS:Our study demonstrated that both epithelial special antigen (ESA) and cytokeratin-20 (CK20) were expressed in LST-R1. The cells presented microvilli and tight junction with large nuclei. The karyotypic analysis showed hyperdiploid features with structural chromosome aberrations. The in vivo tumorigenicity was also demonstrated in nude mice xenograft experiments. The invasion assay suggested this cell line has a higher invasive ability. cDNA microarray and Western blotting show the loss of the expression of E-cadherin in LST-R1 cells.

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The BH3-only protein, PUMA, is involved in oxaliplatin-induced apoptosis in colon cancer cells

Cited by 41 publications

References 33 publications

Taurine induces the apoptosis of breast cancer cells by regulating apoptosis-related proteins of mitochondria

Taurine induces the apoptosis of breast cancer cells by regulating apoptosis-related proteins of mitochondria

Chemosensitisation by manganese superoxide dismutase inhibition is caspase-9 dependent and involves extracellular signal-regulated kinase 1/2

Establishment and characterization of a new cell line derived from human colorectal laterally spreading tumor

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