Retraction: The nuclear export of TR3 mediated gambogic acid-induced apoptosis in cervical cancer cells through mitochondrial dysfunction

Retraction of ‘The nuclear export of TR3 mediated gambogic acid-induced apoptosis in cervical cancer cells through mitochondrial dysfunction’ by Chunhong Zhang et al., RSC Adv., 2019, 9, 11855–11864, DOI: 10.1039/C8RA10542A.

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The nuclear export of TR3 mediated gambogic acid-induced apoptosis in cervical cancer cells through mitochondrial dysfunction

RSC Advances ◽

10.1039/c8ra10542a ◽

2019 ◽

Vol 9 (21) ◽

pp. 11855-11864

Author(s):

Chunhong Zhang ◽

Jia Liu ◽

Fengxing Tao ◽

Yiyi Lu ◽

Qin He ◽

...

Keyword(s):

Cervical Cancer ◽

Mitochondrial Dysfunction ◽

Cancer Cells ◽

Nuclear Export ◽

Gambogic Acid ◽

Cervical Cancer Cells ◽

Induced Apoptosis

The crosstalk of TR3 and p53 mediates GA-induced apoptosis of cervical cancer cells.

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Aesculetin-induced apoptosis through a ROS-mediated mitochondrial dysfunction pathway in human cervical cancer cells

Journal of Asian Natural Products Research ◽

10.1080/10286020903427336 ◽

2010 ◽

Vol 12 (3) ◽

pp. 185-193 ◽

Cited By ~ 28

Author(s):

Jin Yang ◽

Yu-Ling Xiao ◽

Xian-Ran He ◽

Guo-Fu Qiu ◽

Xian-Ming Hu

Keyword(s):

Cervical Cancer ◽

Mitochondrial Dysfunction ◽

Cancer Cells ◽

Cervical Cancer Cells ◽

Induced Apoptosis ◽

Human Cervical Cancer Cells ◽

Human Cervical Cancer

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HP1γ Sensitizes Cervical Cancer Cells to Cisplatin through the Suppression of UBE2L3

International Journal of Molecular Sciences ◽

10.3390/ijms21175976 ◽

2020 ◽

Vol 21 (17) ◽

pp. 5976 ◽

Cited By ~ 1

Author(s):

Sang Ah Yi ◽

Go Woon Kim ◽

Jung Yoo ◽

Jeung-Whan Han ◽

So Hee Kwon

Keyword(s):

Cervical Cancer ◽

Cancer Cells ◽

Nuclear Export ◽

Nuclear Translocation ◽

Leptomycin B ◽

P53 Signaling ◽

Cervical Cancer Cells ◽

Ubiquitin Conjugating Enzyme ◽

The Stability

Cisplatin is the most frequently used agent for chemotherapy against cervical cancer. However, recurrent use of cisplatin induces resistance, representing a major hurdle in the treatment of cervical cancer. Our previous study revealed that HP1γ suppresses UBE2L3, an E2 ubiquitin conjugating enzyme, thereby enhancing the stability of tumor suppressor p53 specifically in cervical cancer cells. As a follow-up study of our previous findings, here we have identified that the pharmacological substances, leptomycin B and doxorubicin, can improve the sensitivity of cervical cancer cells to cisplatin inducing HP1γ-mediated elevation of p53. Leptomycin B, which inhibits the nuclear export of HP1γ, increased cisplatin-dependent apoptosis induction by promoting the activation of p53 signaling. We also found that doxorubicin, which induces the DNA damage response, promotes HP1γ-mediated silencing of UBE2L3 and increases p53 stability. These effects resulted from the nuclear translocation and binding of HP1γ on the UBE2L3 promoter. Doxorubicin sensitized the cisplatin-resistant cervical cancer cells, enhancing their p53 levels and rate of apoptosis when administered together with cisplatin. Our findings reveal a therapeutic strategy to target a specific molecular pathway that contributes to p53 degradation for the treatment of patients with cervical cancer, particularly with cisplatin resistance.

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Abstract 1274: Heterotrimeric stimulatory GTP-binding proteins inhibit cisplatin-induced apoptosis by inducing XIAP in cervical cancer cells

10.1158/1538-7445.am10-1274 ◽

2010 ◽

Author(s):

Eun Ah Cho ◽

Yong-Sung Juhnn

Keyword(s):

Cervical Cancer ◽

Cancer Cells ◽

Binding Proteins ◽

Gtp Binding Proteins ◽

Gtp Binding ◽

Cervical Cancer Cells ◽

Induced Apoptosis

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Hsp90 Inhibitor SNX-2112 Enhances TRAIL-Induced Apoptosis of Human Cervical Cancer Cells via the ROS-Mediated JNK-p53-Autophagy-DR5 Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/9675450 ◽

2019 ◽

Vol 2019 ◽

pp. 1-26

Author(s):

Liubing Hu ◽

Yan Wang ◽

Zui Chen ◽

Liangshun Fu ◽

Sheng Wang ◽

...

Keyword(s):

Cervical Cancer ◽

Cancer Cells ◽

Signaling Pathway ◽

Hela Cells ◽

Cell Apoptosis ◽

Hsp90 Inhibitor ◽

Cervical Cancer Cells ◽

Ros Scavenger ◽

Induced Apoptosis ◽

Human Cervical Cancer

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a potent cancer cell apoptosis-inducing factor that can induce apoptosis in a variety of cancer cells. However, resistance to TRAIL in cancer cells is a huge obstacle in creating effective TRAIL-targeted clinical therapies. Thus, agents that can either enhance the effect of TRAIL or overcome its resistance are needed. In this study, we combined TRAIL with SNX-2112, an Hsp90 inhibitor we previously developed, to explore the effect and mechanism that SNX-2112 enhanced TRAIL-induced apoptosis in cervical cancer cells. Our results showed that SNX-2112 markedly enhanced TRAIL-induced cytotoxicity in HeLa cells, and this combination was found to be synergistic. Additionally, we found that SNX-2112 sensitized TRAIL-mediated apoptosis caspase-dependently in TRAIL-resistant HeLa cells. Mechanismly, SNX-2112 downregulated antiapoptosis proteins, including Bcl-2, Bcl-XL, and FLIP, promoted the accumulation of reactive oxygen species (ROS), and increased the expression levels of p-JNK and p53. ROS scavenger NAC rescued SNX-2112/TRAIL-induced apoptosis and suppressed SNX-2112-induced p-JNK and p53. Moreover, SNX-2112 induced the upregulation of death-receptor DR5 in HeLa cells. The silencing of DR5 by siRNA significantly decreased cell apoptosis by the combined effect of SNX-2112 and TRAIL. In addition, SNX-2112 inhibited the Akt/mTOR signaling pathway and induced autophagy in HeLa cells. The blockage of autophagy by bafilomycin A1 or Atg7 siRNA abolished SNX-2112-induced upregulation of DR5. Meanwhile, ROS scavenger NAC, JNK inhibitor SP600125, and p53 inhibitor PFTα were used to verify that autophagy-mediated upregulation of DR5 was regulated by the SNX-2112-stimulated activation of the ROS-JNK-p53 signaling pathway. Thus, the combination of SNX-2112 and TRAIL may provide a novel strategy for the treatment of human cervical cancer by overcoming cellular mechanisms of apoptosis resistance.

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