ASPP2 Plays a Dual Role in gp120-Induced Autophagy and Apoptosis of Neuroblastoma Cells

Liu, Zhiying; Qiao, Li; Zhang, Yulin; Zang, Yunjing; Shi, Ying; Li, Kai; Zhang, Xin; Lu, Xiaofan; Lin, Yuan; Su, Bin; Zhang, Tong; Wu, Hao; Chen, Dexi

doi:10.3389/fnins.2017.00150

Cited by 14 publications

(15 citation statements)

References 39 publications

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“…One study indicated that ASPP2 could promote Ras-induced senescence through the direct interaction of its N-terminus with Ras-GTP (9). Furthermore, it serves as a pivotal regulator of cell polarity and the autophagy process (10,11). ASPP2 has also been confirmed to bind and co-localize with PAR3, thereby inhibiting tumor metastasis as a molecular switch of epithelial-mesenchymal transition (EMT), and the reduction of ASPP2 results in the poor survival and prognosis of patients with hepatocellular carcinoma and breast cancer (12).…”

Section: Introductionmentioning

confidence: 99%

Silencing of ASPP2 promotes the proliferation, migration and invasion of triple-negative breast cancer cells via the PI3K/AKT pathway

Song

Xie

et al. 2018

Int J Oncol

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Apoptosis-stimulating p53 protein 2 (ASPP2) is an apoptosis inducer that acts via binding with p53 and then enhancing the transcriptional activities toward pro‑apoptosis genes. ASPP2 has recently been reported to serve a major role in p53‑independent pathways. Triple‑negative breast cancer (TNBC) is a type of breast cancer that is more aggressive and highly lethal when p53 is mutated. In the present study, the mRNA level of ASPP2 was found to be suppressed in breast tumors compared with that in adjacent normal breast tissues, and the expression of ASPP2 was also decreased in a series of breast cancer cell lines compared with that in MCF‑10A normal breast cells. Downregulation of ASPP2 by specific small interfering RNA (siRNA) transfection was able to promote cell growth, reduce cell apoptosis, and contribute to cell migration and invasion. Furthermore, downregulation of ASPP2 promoted cell epithelial‑mesenchymal transition (EMT) in MDA‑MB‑231 and HCC‑1937 TNBC cells. Furthermore, it was found that when ASPP2 siRNA was transfected into MDA‑MB‑231 and HCC‑1937 cells, the expression of phosphoinositide‑3‑kinase regulatory subunit 1 (p85α) decreased and phosphorylation of protein kinase B (AKT) increased, which are key molecular regulators in the phosphatidylinositol 3-kinase (PI3K)/AKT pathway. In conclusion, the present data indicated that ASPP2 had a crucial influence on the proliferation and metastasis in TNBC, and that the functional mechanism may be p53‑independent to a great extent. ASPP2 and its link with the PI3K/AKT pathway deserve further investigation and may provide novel insights into therapeutic targets for TNBC.

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Section: Introductionmentioning

confidence: 99%

Silencing of ASPP2 promotes the proliferation, migration and invasion of triple-negative breast cancer cells via the PI3K/AKT pathway

Song

Xie

et al. 2018

Int J Oncol

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“…As a member of ASPP family, the function of ASPP2 is potentially controlled by its binding partners and localisation. When ASPP2 locates at the cytosol/nucleus, ASPP2 enhances p53‐induced apoptosis in cancer cells [15,18,19], whereas in the cell junctions, it binds and maintains the integrity of cell polarity and adherence junction via its N‐terminus [20,21]. In this study, ASPP2 protein was stained with green fluorescence, which was expressed in the perinuclear cytoplasm and/or the nucleus in ESCC cells by immunofluorescence.…”

Section: Discussionmentioning

confidence: 78%

Expression and significance of ASPP2 in squamous carcinoma of esophagus

Liu

et al. 2018

The Kaohsiung J of Med Scie

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To study the significance of apoptosis stimulating protein of P53 2 (ASPP2) expression in esophageal squamous cell carcinoma (ESCC), immunohistochemistry S-P method was used to examine the expression of ASPP2 in 136 cases of ESCC, 35 cases of high grade intraepithelial neoplasia (HGIN), 29 cases of low grade intraepithelial neoplasia (LGIN) and 37 cases of normal esophageal epithelium (NEE). The associations of ASPP2 expression with clinicopathological data and overall survival (OS) were also analyzed. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate ASPP2 expression in a total of 20 matched human ESCC tumor tissues and normal adjacent tissues (NAT). In addition, EC109 cells were treated with cisplatin (CDDP) in vitro for 24 h (the intervention group) and the control group was set up at the same time. Western blot was used to examine the expression of ASPP2 protein between the two groups. The expression of ASPP2 decreased progressively from NEE to LGIN, to HGIN, and to ESCC, and it was related to TNM stage, histological differentiation and lymph node metastasis in ESCC (P < 0.05). ASPP2 was a protective factor of patients with ESCC (P = 0.008). The relative expression of ASPP2 mRNA was markedly downregulated in ESCC compared with the paired NAT (P < 0.01). Western blot results showed that cells in the intervention group could express ASPP2 while there was no expression of ASPP2 in the control group. Taken together, these results indicate that the abnormal expression of ASPP2 may play an important role for development and metastasis in ESCC.

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“…It is a common knowledge that HIV induces T‐cell apoptosis . Several studies have shown that HIV‐1 and its molecules (gp120, Nef) can also mediate neuroblastoma, breast, colorectal, prostate cancer cell growth inhibition and apoptosis. An interesting possibility, explaining lower frequency of several cancers in HIV‐infected persons, is that the HAART drugs can possess cancer‐prevention or antineoplastic activity.…”

Section: Hiv and Cancer Risks In The Haart Eramentioning

confidence: 99%

HIV‐1, HAART and cancer: A complex relationship

Шмакова

Germini

Vassetzky

2019

Intl Journal of Cancer

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HIV infected people are at higher risk of developing cancer, although it is globally diminished in the era of highly active antiretroviral treatment (HAART). Recently, antioncogenic properties of some HAART drugs were discovered. We discuss the role of HAART in the prevention and improvement of treatment outcomes of cancers in HIV‐infected people. We describe different trends in HAART–cancer relationships: cancer‐predisposing as well as cancer‐preventing. We cover the roles of particular drug regimens in cancer prevention. We also describe the causes of cancer treatment with HAART drugs in HIV‐negative people, including ongoing clinical studies that may directly point to a possible independent anti‐oncogenic activity of HAART drugs. We conclude that despite potent antioncogenic activities of every class of HAART drugs reported in preclinical models, the evidence to date indicates that their independent clinical impact in HIV‐infected people is limited. Improved cancer prevention strategies besides HAART are needed to reduce HIV‐cancer‐related mortality.

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ASPP2 Plays a Dual Role in gp120-Induced Autophagy and Apoptosis of Neuroblastoma Cells

Cited by 14 publications

References 39 publications

Silencing of ASPP2 promotes the proliferation, migration and invasion of triple-negative breast cancer cells via the PI3K/AKT pathway

Silencing of ASPP2 promotes the proliferation, migration and invasion of triple-negative breast cancer cells via the PI3K/AKT pathway

Expression and significance of ASPP2 in squamous carcinoma of esophagus

HIV‐1, HAART and cancer: A complex relationship

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