<scp>ASPP</scp>2 enhances Oxaliplatin (L‐<scp>OHP</scp>)‐induced colorectal cancer cell apoptosis in a p53‐independent manner by inhibiting cell autophagy

Shi, Ying; Han, Yanyan; Xie, Fang; Wang, Anna; Feng, Xiaokun; Li, Ning; Guo, Hongbo; Chen, Dexi

doi:10.1111/jcmm.12435

Cited by 35 publications

(43 citation statements)

References 32 publications

(44 reference statements)

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“…It has been reported that NFR2 functions as a suppressor in carcinomas through autophagy-related [38] and inflammation-related cancer signaling pathways [39, 40]. Mounting evidence has suggested that ASPP2 also plays an antitumor role in malignancies through autophagy- [18] and inflammatory-related pathways independent of P53 [19]. Thus, we suggest that ASPP2 may function through similar pathways to NRF2.…”

Section: Discussionmentioning

confidence: 60%

“…High ASPP2 expression has been reported to predict good prognosis in some tumors, including breast cancer [15], non-small cell lung cancer [16], diffuse large B cell lymphoma, and follicular center lymphoma [17]. Moreover, a recent study showed that ASPP2 also induced apoptosis through a P53-independent mechanism [18]. Additionally, ASPP2 plays an important role in regulating the nuclear factor kappa B subunit 1 (NFκB1) inflammatory pathway [19] and in modulating autophagy [18, 20] and cell polarity [21, 22].…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, a recent study showed that ASPP2 also induced apoptosis through a P53-independent mechanism [18]. Additionally, ASPP2 plays an important role in regulating the nuclear factor kappa B subunit 1 (NFκB1) inflammatory pathway [19] and in modulating autophagy [18, 20] and cell polarity [21, 22]. …”

Section: Introductionmentioning

confidence: 99%

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Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

et al. 2017

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BackgroundEsophageal squamous cell carcinoma (ESCC) is a leading cause of cancer-related death, and new prognostic biomarkers are urgently needed. Apoptosis-stimulating P53-binding protein 1 (ASPP1) and 2 (ASPP2) have been reported to play important roles in the development, progression, metastasis, and prognosis of cancers, but their roles in ESCC have not been elucidated. In this study, we examined the expression of ASPP1 and ASPP2 in ESCC to evaluate their prognostic values.MethodsThe protein expression of ASPP1, ASPP2, and P53 in 175 specimens of ESCC was detected using immunohistochemical staining; their expression in cancerous and noncancerous tissues was scored according to the staining intensity and the percentage of stained cells. The associations of ASPP1, ASPP2, and P53 with clinicopathologic parameters, overall survival (OS), and disease-free survival (DFS) were analyzed.ResultsThe protein expression levels of ASPP2 and P53 were significantly higher in cancerous tissues than in paired noncancerous tissues (P < 0.001), whereas the expression levels of ASPP1 in the two groups were similar. In ESCCs, ASPP1 expression was significantly associated with histological differentiation (P = 0.002) and invasive depth (P = 0.014); ASPP2 expression was associated with age (P = 0.029) and histological differentiation (P < 0.001); and P53 expression was associated with age (P = 0.021) and tumor size (P = 0.040). No correlations were found between ASPP1, ASPP2, and P53 expression. Survival analysis revealed that high ASPP2 expression was significantly associated with increased 5-year OS (P = 0.001) and DFS rates (P = 0.010) and that high P53 expression was significantly associated with a reduced 5-year DFS rate of ESCC patients (P = 0.015). Multivariate Cox analysis indicated that ASPP2 was an independent predictor of OS [hazard ratio (HR): 0.541, 95% confidence interval (CI) 0.363–0.804] and DFS (HR: 0.599, 95% CI 0.404–0.888) of ESCC patients and that P53 was an independent predictor of DFS (HR: 2.161, 95% CI 1.100–4.245).ConclusionsASPP1 might be involved in the progression of ESCC, and ASPP2 was a potential prognostic biomarker of ESCC and should be evaluated in future studies.

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Section: Discussionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 99%

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Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

et al. 2017

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“…Lycorine also induced apoptosis in MM cell regardless of genetic variation (Supplementary Figure S1). To check whether autophagy contributes to MM cell growth and whether autophagy inhibition contributes to lycorine anti-MM function, the autophagy inhibitor 3-Methyladenine (3-MA) was applied 34. 3-MA treatment led to a significant decreased viability of both cell lines ( p <0.01).…”

Section: Resultsmentioning

confidence: 99%

Lycorine Downregulates HMGB1 to Inhibit Autophagy and Enhances Bortezomib Activity in Multiple Myeloma

Roy¹,

Liang²,

Xiao³

et al. 2016

Theranostics

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Multiple myeloma (MM) is largely incurable and drug-resistant. Novel therapeutic approaches such as inhibiting autophagy or rational drug combinations are aimed to overcome this issue. In this study, we found that lycorine exhibits a promising anti-proliferative activity against MM in vitro and in vivo by inhibiting autophagy. We identified High mobility group box 1 (HMGB1), an important regulator of autophagy, as the most aberrantly expressed protein after lycorine treatment and as a critical mediator of lycorine activity. Gene expression profiling (GEP) analysis showed that higher expression of HMGB1 is linked with the poor prognosis of MM. This correlation was further confirmed in human bone marrow CD138+ primary myeloma cells and MM cell lines. Mechanistically, proteasomal degradation of HMGB1 by lycorine inhibits the activation of MEK-ERK thereby decreases phosphorylation of Bcl-2 resulting in constitutive association of Bcl-2 with Beclin-1. In addition, we observed higher HMGB1 expression in bortezomib resistant cells and the combination of bortezomib plus lycorine was highly efficient in vitro and in vivo myeloma models as well as in re-sensitizing resistant cells to bortezomib. These observations indicate lycorine as an effective autophagy inhibitor and reveal that lycorine alone or in combination with bortezomib is a potential therapeutic strategy.

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“…EGFR can reduce ASPP2-induced apoptosis by the activation of the PI3K/Akt signaling pathway in hepatoma cells [14]. In colorectal cancer cells, ASPP2 induces apoptosis by binding and activating the RAS/PI3K/AKT signaling pathway [15, 16]. Therefore, the PI3K/Akt signaling pathway plays a critical role in tumor cell apoptosis and the discovery of lung cancer targeted drugs.…”

Section: Introductionmentioning

confidence: 99%

Effect of miR-21 on Apoptosis in Lung Cancer Cell Through Inhibiting the PI3K/ Akt/NF-κB Signaling Pathway in Vitro and in Vivo

Zhou

Wang

Sun

et al. 2018

Cell Physiol Biochem

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Background/Aims: Lung cancer is one of the most common malignancies in the world. Apoptosis-stimulating protein of p53 (ASPP2), a tumorigenesis related protein, plays a critical role in the initiation and development of various types of cancers. However, the effect of ASPP2 on lung cancer remains unknown. The purpose of this study aims to investigate the mechanism of ASPP2 regulated by miR-21 in lung cancer in vitro and in vivo. Methods: In the study, migration and invasion assays, apoptosis assay, caspase activity assay, TUNEL staining, real time PCR and western blot were used to investigate the mechanism of ASPP2 regulated by miR-21 in lung cancer in vitro and in vivo. Results: We demonstrated that the miR-21 inhibitor induced apoptosis through inhibiting the PI3K/Akt/NF-κB signaling pathway in non-small cell lung carcinoma (NSCLC). Moreover, ASPP2 was directly targeted by miR-21 in NSCLC cells. Down-regulation of miR-21 suppressed cell migration and invasion, as well as the EMT signaling pathway in NSCLC cells. Furthermore, the miR-21 inhibitor induced cell apoptosis via the caspase dependent pathway in NSCLC cells. The miR-21 inhibitor enhanced caspase-3, 8, 9 activity in NSCLC cells. In addition, the caspase inhibitor significantly reduced the apoptosis induced by the miR-21 inhibitor in NSCLC cells. Conclusions: Our results revealed that the miR-21 inhibitor could induce apoptosis through inhibiting the PI3K/Akt/NF-κB signaling pathway in human NSCLC cells, and might serve as a therapeutic strategy to treat NSCLC.

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ASPP2 enhances Oxaliplatin (L‐OHP)‐induced colorectal cancer cell apoptosis in a p53‐independent manner by inhibiting cell autophagy

Cited by 35 publications

References 32 publications

Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

Prognostic values of apoptosis-stimulating P53-binding protein 1 and 2 and their relationships with clinical characteristics of esophageal squamous cell carcinoma patients: a retrospective study

Lycorine Downregulates HMGB1 to Inhibit Autophagy and Enhances Bortezomib Activity in Multiple Myeloma

Effect of miR-21 on Apoptosis in Lung Cancer Cell Through Inhibiting the PI3K/ Akt/NF-κB Signaling Pathway in Vitro and in Vivo

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