Reactive oxygen species burst induced by aluminum stress triggers mitochondria-dependent programmed cell death in peanut root tip cells

Huang, Wenjing; Yang, Xudong; Yao, Shaochang; Lwin-Oo, Thet; He, Hua; Wang, Aiqin; ChuangZhen, Li; He, Long-Fei

doi:10.1016/j.plaphy.2014.03.037

Cited by 86 publications

(61 citation statements)

References 42 publications

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“…Caspase-3 is a member of the caspase (cysteine aspartic proteinases) family of enzymes, which are the major inducers of apoptosis. Caspase-3 is activated in the apoptotic cell both by extrinsic (death ligand) and intrinsic (mitochondrial) pathways (Huang et al, 2014). One signaling event is the introduction of granzyme B, which can activate initiator caspases, into cells targeted for apoptosis by killer T cells.…”

Section: Discussionmentioning

confidence: 99%

Effects of PLCE1 Gene Silencing by RNA Interference on Cell Cycling and Apoptosis in Esophageal Carcinoma Cells

Zhao¹,

Wei²,

Yang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Esophageal squamous cell carcinoma (ESCC) is one of the most malignancies with a poor prognosis. The phospholipase Cε gene (PLCE1) encodes a novel ras-related protein effector mediating the effects of R-Ras on the actin cytoskeleton and membrane protrusion. However, molecular mechanisms pertinent to ESCC are unclear. We therefore designed PLCE1-special small interfering RNA and transfected to esophageal squamous cell (EC) 9706 cells to investigat the effects of PLCE1 gene silencing on the cell cycle and apoptosis of ESCC and indicate its important role in the development of ESCC. Esophageal cancer tissue specimens and normal esophageal mucosa were obtained and assayed by immunohistochemical staining to confirm overexpression of PLCE1 in neoplasias. Fluorescence microscopy was used to examine transfection efficiency, while the result of PLCE1 silencing was examined by reverse transcription (RT-PCR). Flow cytometry and annexin V apoptosis assays were used to assess the cell cycle and apoptosis, respectively. Expression of cyclin D1 and caspase-3 was detected by Western-blotting. The level of PLCE1 protein in esophageal cancer tissue was significantly higher than that in normal tissue. After transfection, the expression of PLCE1 mRNA in EC 9706 was significantly reduced, compared with the control group. Furthermore, flow cytometry results suggested that the PLCE1 gene silencing arrested the cell cycle in the G0/G1 phase; apoptosis was significantly higher than in the negative control group and mock group. PLCE1 gene silencing by RNAi resulted in decreased expression of cyclin D1 and increased expression of caspase-3. Our study suggests that PLCE1 may be an oncogene and play an important role in esophageal carcinogenesis through regulating proteins which control cell cycling and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Effects of PLCE1 Gene Silencing by RNA Interference on Cell Cycling and Apoptosis in Esophageal Carcinoma Cells

Zhao¹,

Wei²,

Yang³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…By contrast, caspase-3 is a member of the caspase family of enzymes, which are the major inducers of apoptosis (21). This apoptotic protein is identified as one of the mechanisms by which cancer cells accelerate apoptosis, and is activated in the apoptotic cell by extrinsic (death ligand) and intrinsic (mitochondrial) pathways (22). The present study revealed that silencing the TSPAN1 gene by siRNA resulted in an increase in caspase-3 expression, consequently promoting the apoptosis of EC.…”

Section: Discussionmentioning

confidence: 99%

Expression and function of tetraspanin 1 in esophageal carcinoma

Chen

et al. 2017

Oncol Lett

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Abstract. The present study explored the expression of tetraspanin 1 (TSPAN1) in esophageal carcinoma (EC) and its association with clinicopathological factors. TSPAN1 small interfering RNA (siRNA) was designed to target the TSPAN1 gene in Eca-109 cells in order to explore the biological function of TSPAN1 in the proliferation and apoptosis of EC. The results demonstrated that the level of TSPAN1 expression in EC tissue was significantly increased compared with that in adjacent normal tissue (P<0.001). TSPAN1 expression was also associated with histological differentiation, depth of invasion, lymph node metastasis (all P<0.05) and Ki-67 (P<0.01). However, no association was observed between TSPAN expression and gender, age or location (P>0.05). In addition, silencing TSPAN1 markedly inhibited proliferation while increasing the apoptosis rate of Eca-109 cells, which was demonstrated by detecting the expression of the cell proliferation-associated gene Ki-67 and the apoptotic gene caspase-3 (P<0.05). Taken together, these results indicated that TSPAN1 functions as a tumor-associated gene in EC through promoting cell proliferation and suppressing apoptosis, and siRNA technology may provide an advanced alternative in the development of therapeutics for EC. IntroductionEsophageal carcinoma (EC) is one of the most fatal cancers of the digestive system worldwide (1). Although great improvements have been made in the diagnosis and surgical treatment of EC, the overall survival rate remains poor (2). Therefore, it is necessary to study the molecular mechanisms of the development of EC. In particular, studying the role of the new tumor-associated genes in EC may help to elucidate the mechanisms of EC initiation and progression, and provide effective targets for treatment of EC. Tetraspanin 1 (TSPAN1; GenBank accession no., AF065388; also termed NET-1), which encodes a 241 amino acid protein and is located at chromosome 1p34.1, belongs to the tetraspanin superfamily (TM4SF) and was identified by Serru et al (3) from the EST database in 2000. TM4SF, a specific family member of cell membrane glycoproteins, is widely expressed in numerous tissues and cells and mediates extracellular signal transduction and performs an important role in cell development, growth and movement through the role of the four hydrophobic regions in determining the boundaries of extracellular transmembrane regions of cysteine residues (4).Previous studies revealed that TSPAN1 was highly expressed in a number of cancers (5,6), but the role of TSPAN1 in EC was unclear. In addition, it was also uncertain whether TSPAN1 affects the proliferation and apoptosis of EC cells. Therefore, the present study detected TSPAN1 protein in EC tissues and evaluated its association with clinicopathological factors and progression of EC. The effects of target inhibiting TSPAN1 with siRNA on the EC cells were examined, and the effects on proliferation and apoptosis of EC cells were observed. Materials and methods Patients.A total of 60 samples of EC tissue from resected s...

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“…Accumulation of Al occurred at root meristems and as a result inhibition of root elongation was the first sign of Al toxicity [7,36,39]. It was reported that inhibition of root elongation of Leucaena leucocephala [28] and peanut [40] achieved at 30 µM and 100 µM Al respectively. The reduced growth of roots might be caused by the Al toxicity which affect the plasma membrane of the root cells at the root apex, inhibit cell division and cell extension [5].…”

Section: Discussionmentioning

confidence: 99%

Untitled

2017

JESR

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Abstract:Being the most abundant element on earth, aluminium has become one of the major restricting factors that affect the growth and development of plants. The first target of aluminium toxicity is the root apex which would in turn affect the overall growth of the plants. In this study, the effect of various concentrations of aluminium (Al) on the growth of Lobelia chinensis was determined. Nodal explants of L. chinensis were cultured on MS medium containing various concentrations of aluminium chloride (AlCl3) (0, 1.0, 2.5, 5.0, 7.5, 10.0 and 20 µM) with 1250.0 μM ion phosphate and pH was adjusted to 4.6. It was observed that both the growth of shoot and root decreased with the increasing concentrations of Al.

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Reactive oxygen species burst induced by aluminum stress triggers mitochondria-dependent programmed cell death in peanut root tip cells

Cited by 86 publications

References 42 publications

Effects of PLCE1 Gene Silencing by RNA Interference on Cell Cycling and Apoptosis in Esophageal Carcinoma Cells

Effects of PLCE1 Gene Silencing by RNA Interference on Cell Cycling and Apoptosis in Esophageal Carcinoma Cells

Expression and function of tetraspanin 1 in esophageal carcinoma

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