The effect of p66shc protein on the resistance of the RKO colon cancer cell line to oxidative stress

Galimov, Evgeniy R.; Sidorenko, A. S.; Tereshkova, A. V.; Pletyushkina, O.; Chernyak, Boris V.; Chumakov, P. M.

doi:10.1134/s0026893312010062

Cited by 11 publications

(8 citation statements)

References 47 publications

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“…This suggests that p66Shc is specifically relevant to the pathogenesis of DN. In addition, several different studies have indicated that p66Shc is involved in various chronic diseases that are secondarily due to oxidative damage 9 10 11 12 . Furthermore, there are many in vivo and in vitro studies implicating p66Shc in the progression of DN via the modulation of mitochondrial ROS production, leading to oxidative stress in the kidney 13 14 .…”

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confidence: 99%

p66Shc: A novel biomarker of tubular oxidative injury in patients with diabetic nephropathy

Zhu

et al. 2016

Sci Rep

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Increased p66Shc expression has been associated with diabetic nephropathy (DN). However, whether p66Shc can serve as a potential biomarker for tubular oxidative injury in DN is unknown. We measured the expression of p66Shc in peripheral blood monocytes (PBMs) and renal biopsy tissues from DN patients and then analysed the relationship between p66Shc expression and the clinical characteristics of patients with DN. Patients were divided into 4 groups (class IIa, class IIb, class III and the control group). qPCR, Western blotting and immunohistochemistry were performed. The results showed that both p66Shc and p-p66Shc expression significantly increased in PBMs and kidney tissues of DN patients. Moreover, Spearman’s correlation and multiple regression analyses were carried out. A positive relationship between the p66Shc expression and oxidative stress was found. p66Shc and oxidative stress were significant predictors of the degree of tubular damage. In addition, p66Shc expression was positively correlated with the concentrations of β-NAG, UACR and 8-OHdG, low-density lipoprotein and blood glucose levels, and duration of diabetes in patients with DN from class IIa to class III. These data indicated that increased expression of p66Shc may serve as a therapeutic target and a novel biomarker of DN.

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confidence: 99%

p66Shc: A novel biomarker of tubular oxidative injury in patients with diabetic nephropathy

Zhu

et al. 2016

Sci Rep

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“…Colorectal carcinoma cells (RKO) have been characterized to exhibit increased p66Shc levels and hydrogen peroxide production, which lead to mitochondrial fragmentation and cell death, in vitro. Increased p66Shc levels have also been found in colon cancers [36], while decreased p66Shc protein levels have been found in human lung cancers [19,37]. Similarly, Abdollahi et al [38] observed decreased p66Shc expression in malignant ovarian surface epithelial cells compared with control cells.…”

Section: Other Cancersmentioning

confidence: 93%

The interplay between p66Shc, reactive oxygen species and cancer cell metabolism

Lebiedzińska-Arciszewska

Oparka

Vega‐Naredo

et al. 2014

Eur J Clin Investigation

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The adaptor protein p66Shc links membrane receptors to intracellular signalling pathways and has the potential to respond to energy status changes and regulate mitogenic signalling. Initially reported to mediate growth signals in normal and cancer cells, p66Shc has also been recognized as a pro-apoptotic protein involved in the cellular response to oxidative stress. Moreover, it is a key element in processes such as cancer cell proliferation, tumor progression, metastasis and metabolic reprogramming. Recent findings on the role of p66Shc in the above-mentioned processes have been obtained through the use of various tumor cell types, including prostate, breast, ovarian, lung, colon, skin and thyroid cancer cells. Interestingly, the impact of p66Shc on the proliferation rate was mainly observed in prostate tumors, while its impact on metastasis was mainly found in breast cancers. In this review, we summarize the current knowledge about the possible roles of p66Shc in different cancers. Keywords Cancer, cancer metabolism, p66Shc, reactive oxygen species.Eur J Clin Invest 2015; 45 (S1): 25-31The role of p66Shc in the cellular response to oxidative stress p66Shc has been extensively studied for many years, mostly in the contexts of the cellular response to oxidative stress and the mammalian lifespan. Now, p66Shc is considered to be involved in many other biological and pathological processes. p66Shc belongs to the ShcA family of adaptor proteins that consists of three members: p46Shc, p52Shc and p66Shc, with molecular masses of 46, 52 and 66 kDa, respectively. In humans, all ShcA proteins are encoded by the same gene, localized at chromosome 1q21 [1][2][3]. p66Shc, p52Shc and p46 have similar domain structures and contain three functionally identical domains (the PTB-CH1-SH2 signature): a N-terminal phosphotyrosinebinding domain (PTB), a central proline-rich domain (CH1) and a carboxy terminal Src homology 2 (SH2) domain. In response to growth factor stimuli, p66Shc is phosphorylated at the same tyrosine residues (Y293, Y240 and Y317) as the other two ShcA members (p52Shc and p46Shc) [4,5] but exerts opposite effects, acting as a negative regulator of cell proliferation [6][7][8][9]. Interestingly, p66Shc differs from p52Shc and p46Shc by the presence of an additional N-terminal proline-rich collagen homology domain (CH2), which contains a serine phosphorylation site (Ser36) that is critical for its pro-oxidant properties. Moreover, p66Shc contains a functional region (CCB, a cytochrome c-binding region) within the CH2-PTB domains that is responsible for the interaction of p66Shc with cytochrome c [10]. The intracellular localization of p66Shc remains controversial. Several reports have indicated that this cytosolic adaptor protein exhibits different subcellular localizations. At the plasma membrane, p66Shc is involved in signal transduction that mediates receptor tyrosine kinase signalling (Ras/ MAPK signalling), promotes Rac1 activation and triggers NADPH membrane oxidase reactive oxygen species (ROS) produ...

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“…SHC1 is believed to be involved in inhibiting neuronal apoptosis and regulating the receptor tyrosine kinase pathway [ 10 ]. With further study on SHC1, it has been found that the SHC1 gene plays an important role in the growth of breast cancer [ 11 ], gastrointestinal tumor cells [ 12 , 13 ], and other tumor cells. However, the role of SHC1 in lung cancer needs further study.…”

Section: Introductionmentioning

confidence: 99%

SHC1 Promotes Lung Cancer Metastasis by Interacting with EGFR

Yang

2022

Journal of Oncology

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The study aims to explore the biological function of SHC1 in the development and progression of lung cancer. Meanwhile, the effect of SHC1 and EGFR on lung cancer was analyzed. The expression of SHC1 in lung cancer and adjacent tissues was analyzed by bioinformatics and immunohistochemistry. Meanwhile, the relationship between SHC1 expression and prognosis was analyzed. SHC1 overexpression and knockdown cell lines were constructed by overexpression plasmid and knockdown plasmid. Cell proliferation was detected by CCK-8. Cell invasion was detected by transwell. Apoptosis was detected by TUNEL. Interaction between SHC1 and EGFR was detected. The expression of SHC1 in lung adenocarcinoma tissues was significantly higher than that in paracancer tissues. Lung cancer patients with high SHC1 expression have a poor prognosis. The proliferation and invasion of SHC1 decreased with SHC1 knockout but increased after overexpression. EGFR may be a key interaction protein of SHC1. Overexpression of EGFR increases the oncogenic effect of SHC1. In conclusion, SHC1 plays a carcinogenic role in lung cancer. EGFR expression was significantly correlated with SHC1 and maybe a key interaction protein of SHC1. SHC1 interacts with EGFR to form a protein complex, which may be a new target for lung cancer metastasis.

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The effect of p66shc protein on the resistance of the RKO colon cancer cell line to oxidative stress

Cited by 11 publications

References 47 publications

p66Shc: A novel biomarker of tubular oxidative injury in patients with diabetic nephropathy

p66Shc: A novel biomarker of tubular oxidative injury in patients with diabetic nephropathy

The interplay between p66Shc, reactive oxygen species and cancer cell metabolism

SHC1 Promotes Lung Cancer Metastasis by Interacting with EGFR

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