Effect and mechanism of action of SLP‑2 on the apoptosis and autophagy of gastric cancer cells

Yang, Shengsen; Huang, Yun; Zhang, Hongyan; Wang, Fang; Shao, Liangui; Wang, Xuehong

doi:10.3892/ol.2021.12968

Cited by 4 publications

(3 citation statements)

References 34 publications

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“…Studies have shown that excessive mitochondrial fission can lead to excessive mitophagy, which exacerbates cardiac remodeling, and overexpression of SLP-2 can significantly increase the content of mitochondrial fusion protein Mfn2, thereby reducing mitochondrial fission and oxidative stress injury [48][49][50][51]. Silencing SLP-2 can inhibit gastric cancer cell proliferation and induce apoptosis and autophagy via ANXA2/ β-catenin signal pathway [28]. In our study, the expression levels of LC3B II, Beclin1 and ATG5 in SLP-2 -/-Dox group were significantly higher than WT Dox group, suggesting that SLP-2 deficiency aggravated cardiomyocyte autophagy induced by Dox.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous research suggests that overexpression of SLP-2 reduces cardiomyocyte apoptosis, mitochondrial injury, and myocardial I/R injury [ 27 ]. A study on gastric cancer shows that silencing SLP-2 expression can induce apoptosis and autophagy in cancer cells [ 28 ]. At present, the mechanism of SLP-2 in myocardial fibrosis and cardiomyocyte autophagy remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling

Jiang

et al. 2023

Cell Death Discov.

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Myocardial fibrosis, oxidative stress, and autophagy both play key roles in the progression of adverse cardiac remodeling. Stomatin-like protein 2 (SLP-2) is closely related to mitochondrial function, but little is known about its role and mechanism in cardiac remodeling. We developed doxorubicin (Dox), angiotensin (Ang) II, and myocardial ischemia-reperfusion (I/R) injury induced cardiac remodeling model and Dox treated H9C2 cell injury model using SLP-2 knockout (SLP-2-/-) mice and H9C2 cells with low SLP-2 expression. We first examined cardiac functional and structural changes as well as levels of oxidative stress, apoptosis and autophagy. We found that SLP-2 deficiency leads to decreased cardiac function and promotes myocardial fibrosis. After Dox and Ang II treatment, SLP-2 deficiency further aggravated myocardial fibrosis, increased myocardial oxidative stress and apoptosis, and activated autophagy by inhibiting PI3K-Akt-mTOR signaling pathway, ultimately exacerbating adverse cardiac remodeling. Similarly, SLP-2 deficiency further exacerbates adverse cardiac remodeling after myocardial I/R injury. Moreover, we extracted cardiomyocyte mitochondria for proteomic analysis, suggesting that SLP-2 deficiency may be involved in myocardial I/R injury induced adverse cardiac remodeling by influencing ubiquitination of intramitochondrial proteins. In addition, the oxidative stress, apoptosis and autophagy levels of H9C2 cells with low SLP-2 expression were further enhanced, and the PI3K-Akt-mTOR signaling pathway was further inhibited under Dox stimulation. Our results suggest that SLP-2 deficiency promotes myocardial fibrosis, disrupts normal mitochondrial function, overactivates autophagy via PI3K-Akt-mTOR signaling pathway, affects the level of ubiquitination, leads to irreversible myocardial damage, and ultimately exacerbates adverse cardiac remodeling.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling

Jiang

et al. 2023

Cell Death Discov.

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“…Cellular senescence was demonstrated to influence the bone formation in many studies [ 35 , 36 ]. However, the expression of ANXA2 can be regulated through various substances, including those that are involved with inflammation and cancers [ 37 , 38 ].…”

Section: Discussionmentioning

confidence: 99%

Annexin A2 Improves the Osteogenic Differentiation of Mesenchymal Stem Cells Exposed to High-Glucose Conditions through Lessening the Senescence

Klabklai

Phetfong

Tangporncharoen

et al. 2022

IJMS

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Osteoporosis is frequently found in chronic diabetic patients, and it results in an increased risk of bone fractures occurring. The underlying mechanism of osteoporosis in diabetic patients is still largely unknown. Annexin A2 (ANXA2), a family of calcium-binding proteins, has been reported to be involved in many biological process including bone remodeling. This study aimed to investigate the role of ANXA2 in mesenchymal stem cells (MSCs) during in vitro osteoinduction under high-glucose concentrations. Osteogenic gene expression, calcium deposition, and cellular senescence were determined. The high-glucose conditions reduced the osteogenic differentiation potential of the MSCs along with the lower expression of ANXA2. Moreover, the high-glucose conditions increased the cellular senescence of the MSCs as determined by senescence-associated β-galactosidase staining and the expression of p16, p21, and p53 genes. The addition of recombinant ANXA2 could recover the glucose-induced deterioration of the osteogenic differentiation of the MSCs and ameliorate the glucose-induced cellular senescence of the MSCs. A Western blot analysis revealed an increase in p53 and phosphorylated p53 (Ser 15), which was decreased by recombinant ANXA2 in MSC osteoblastic differentiation under high-glucose conditions. Our study suggested that the alteration of ANXA2 in high-glucose conditions may be one of the plausible factors in the deterioration of bones in diabetic patients by triggering cellular senescence.

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SLP-2 regulates the generation of reactive oxygen species and the ERK pathway to promote papillary thyroid carcinoma motility and angiogenesis

Chen

Wang

et al. 2023

Tissue and Cell

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Effect and mechanism of action of SLP‑2 on the apoptosis and autophagy of gastric cancer cells

Cited by 4 publications

References 34 publications

Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling

Stomatin-like protein 2 deficiency exacerbates adverse cardiac remodeling

Annexin A2 Improves the Osteogenic Differentiation of Mesenchymal Stem Cells Exposed to High-Glucose Conditions through Lessening the Senescence

SLP-2 regulates the generation of reactive oxygen species and the ERK pathway to promote papillary thyroid carcinoma motility and angiogenesis

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