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Dive into the research topics where Hang Cui is active.

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Featured researches published by Hang Cui.


Journal of Signal Transduction | 2012

Oxidative stress, mitochondrial dysfunction, and aging

Hang Cui; Yahui Kong; Hong Zhang

Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.


Cancer Research | 2013

Notch3 Functions as a Tumor Suppressor by Controlling Cellular Senescence

Hang Cui; Yahui Kong; Mei Xu; Hong Zhang

Notch signaling regulates a broad spectrum of cell fate decisions and differentiation. Both oncogenic and tumor suppressor functions have been shown for Notch signaling. However, little is known about the underlying mechanisms of its tumor suppressor function. Here, we report that expression of Notch3, a member of Notch family transmembrane receptors, was elevated in human cells during senescence activated by various senescence-inducing stimuli. This upregulation of Notch3 was required for the induction of p21 expression in senescent cells. Downregulation of Notch3 led to a delayed onset of senescence and extended replicative lifespan, whereas adventitious expression of Notch3 was sufficient to activate senescence and p21 expression. The ability of Notch3 to induce senescence and p21 expression was dependent on the canonical Notch singling. Deletion of p21 in cells significantly attenuated Notch3-induced senescence. Furthermore, a significant decrease in Notch3 expression was observed in human tumor cell lines as well as primary human breast cancer and melanoma samples compared with normal tissues. Restoration of Notch3 expression in human tumor cells resulted in inhibition of cell proliferation and activation of senescence. Collectively, our results reveal a novel function of Notch3 in senescence regulation and tumor suppression.


Journal of Aging Research | 2011

Regulation of Senescence in Cancer and Aging

Yahui Kong; Hang Cui; Charusheila Ramkumar; Hong Zhang

Senescence is regarded as a physiological response of cells to stress, including telomere dysfunction, aberrant oncogenic activation, DNA damage, and oxidative stress. This stress response has an antagonistically pleiotropic effect to organisms: beneficial as a tumor suppressor, but detrimental by contributing to aging. The emergence of senescence as an effective tumor suppression mechanism is highlighted by recent demonstration that senescence prevents proliferation of cells at risk of neoplastic transformation. Consequently, induction of senescence is recognized as a potential treatment of cancer. Substantial evidence also suggests that senescence plays an important role in aging, particularly in aging of stem cells. In this paper, we will discuss the molecular regulation of senescence its role in cancer and aging. The potential utility of senescence in cancer therapeutics will also be discussed.


Aging Cell | 2011

Smurf2-mediated ubiquitination and degradation of Id1 regulates p16 expression during senescence

Yahui Kong; Hang Cui; Hong Zhang

The inhibitor of differentiation or DNA binding (Id) family of transcription regulators plays an important role in cell proliferation, differentiation, and senescence. However, regulation of Id expression during these processes is poorly understood. Id proteins are known to undergo rapid turnover mediated by the ubiquitin‐proteasome pathway. Anaphase‐promoting complex has been shown to ubiquitinate Id2, but E3 ubiquitin ligase(s) that ubiquitinate other Id family members are not known. Here, we report for the first time the identification of Smurf2 as the E3 ligase that ubiquitinates Id1 and Id3. Smurf2‐mediated ubiquitination and consequent degradation of Id1 or Id3 plays an important role in the regulation of Id expression in senescent cells. Furthermore, we found that Id1 is the mediator through which Smurf2 regulates p16 expression, providing a mechanistic link between Smurf2 and p16 expression during senescence.


Nature Communications | 2013

Smurf2 suppresses B-cell proliferation and lymphomagenesis by mediating ubiquitination and degradation of YY1

Charusheila Ramkumar; Hang Cui; Yahui Kong; Stephen N. Jones; Rachel M. Gerstein; Hong-Hong Zhang

About half of patients with diffuse large B-cell lymphoma (DLBCL) do not respond to or relapse soon after the standard chemotherapy, indicating a critical need to better understand the specific pathways perturbed in DLBCL for developing effective therapeutic approaches. Mice deficient in the E3 ubiquitin ligase Smurf2 spontaneously develop B-cell lymphomas that resemble human DLBCL with molecular features of germinal center or post-germinal center B cells. Here we show that Smurf2 mediates ubiquitination and degradation of YY1, a key germinal center transcription factor. Smurf2 deficiency enhances YY1-mediated transactivation of c-Myc and B-cell proliferation. Furthermore, Smurf2 expression is significantly decreased in primary human DLBCL samples, and low levels of Smurf2 expression correlate with inferior survival in DLBCL patients. The Smurf2-YY1-c-Myc regulatory axis represents a novel pathway perturbed in DLBCL that suppresses B-cell proliferation and lymphomagenesis, suggesting pharmaceutical targeting of Smurf2 as a new therapeutic paradigm for DLBCL.


Oncotarget | 2016

Targeting the chromatin remodeling enzyme BRG1 increases the efficacy of chemotherapy drugs in breast cancer cells

Qiong Wu; Soni Sharma; Hang Cui; Scott E. LeBlanc; Hong Zhang; Rohini Muthuswami; Jeffrey A. Nickerson; Anthony N. Imbalzano

Brahma related gene product 1 (BRG1) is an ATPase that drives the catalytic activity of a subset of the mammalian SWI/SNF chromatin remodeling enzymes. BRG1 is overexpressed in most human breast cancer tumors without evidence of mutation and is required for breast cancer cell proliferation. We demonstrate that knockdown of BRG1 sensitized triple negative breast cancer cells to chemotherapeutic drugs used to treat breast cancer. An inhibitor of the BRG1 bromodomain had no effect on breast cancer cell viability, but an inhibitory molecule that targets the BRG1 ATPase activity recapitulated the increased drug efficacy observed in the presence of BRG1 knockdown. We further demonstrate that inhibition of BRG1 ATPase activity blocks the induction of ABC transporter genes by these chemotherapeutic drugs and that BRG1 binds to ABC transporter gene promoters. This inhibition increased intracellular concentrations of the drugs, providing a likely mechanism for the increased chemosensitivity. Since ABC transporters and their induction by chemotherapy drugs are a major cause of chemoresistance and treatment failure, these results support the idea that targeting the enzymatic activity of BRG1 would be an effective adjuvant therapy for breast cancer.


Cancer Research | 2013

Abstract 1994: Smurf2 mediates ubiquitination and degradation of YY1 to suppress B-cell proliferation and lymphomagenesis.

Charusheila Ramkumar; Hang Cui; Yahui Kong; Stephen N. Jones; Rachel M. Gerstein; Hong Zhang

Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC Current treatment of diffuse large B-cell lymphoma (DLBCL), the most common type of non-Hodgkins lymphoma, has improved patient survival significantly. However, 40-50% of DLBCL patients still die from this disease. There is a critical need to better understand the specific molecular pathways that are perturbed in DLBCL for the development of new and effective therapeutic approaches. We show that mice deficient in the E3 ubiquitin ligase Smurf2 spontaneously develop B-cell lymphomas that resemble human DLBCL with molecular features of germinal center B cells. We discover that Smurf2 mediates ubiquitination and degradation of YY1, a key germinal center transcription factor. Importantly, Smurf2 deficiency enhances YY1-mediated transactivation of c-Myc and B-cell proliferation. Furthermore, the expression of Smurf2 is significantly decreased in primary human DLBCL samples compared to normal B cells, and low levels of Smurf2 expression correlate with poor survival prognosis in DLBCL patients. The Smurf2-YY1-c-Myc regulatory axis represents a novel pathway perturbed in DLBCL that suppresses B-cell proliferation and lymphomagenesis, suggesting Smurf2 as a new therapeutic paradigm for DLBCL. Citation Format: Charusheila Ramkumar, Hang Cui, Yahui Kong, Stephen Jones, Rachel Gerstein, Hong Zhang. Smurf2 mediates ubiquitination and degradation of YY1 to suppress B-cell proliferation and lymphomagenesis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1994. doi:10.1158/1538-7445.AM2013-1994 Note: This abstract was not presented at the AACR Annual Meeting 2013 because the presenter was unable to attend.


Cancer Research | 2011

Abstract 1240: Characterization of Notch3 in senescence regulation and tumor suppression

Hang Cui; Hong Zhang

Notch signaling has been shown to regulate a broad spectrum of cell fate decisions and differentiation. However, very little is known about the role of Notch signaling in cellular senescence. Here we report that the level of Notch3, a member of Notch transmembrane receptors, is specifically elevated in human fibroblasts during senescence induced by different senescence stimuli. This up-regulation of Notch3 is required for the induction of p21 in senescent cells, whereas adventitious expression of Notch3 in early passage fibroblasts induces senescence accompanied by p21 elevation. Furthermore, we find that Notch3-mediated senescence requires a canonic Notch singling, and deletion of p21 can partially abolish Notch3-induced senescence. The expression of Notch3 is undetectable in a number of human cancer cell lines, and restored expression of Notch3 in these cancer cell lines with undetectable level of Notch3 leads to proliferative arrest. Interestingly, the expression of Notch3 in the luminal subtype of human breast cancer is significantly decreased as compared to other subtypes of breast cancer. More importantly, low level of Notch3 expression in patients with luminal type of breast cancer correlates significantly with poor clinical prognosis. Our results reveal a novel function of Notch3 in senescence regulation and tumor suppression, suggesting that modulation of Notch3 provides a potential therapeutic approach for luminal subtype of breast cancer. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1240. doi:10.1158/1538-7445.AM2011-1240


Journal of Immunology | 2013

Smurf2 mediates ubiquitination and degradation of YY1 to suppress B-cell proliferation and lymphomagenesis (P2181)

Rachel M. Gerstein; Charusheila Ramkumar; Hang Cui; Yahui Kong; Stephen N. Jones; Hong Zhang


Journal of Immunology | 2012

The E3 ubiquitin ligase Smurf2 suppresses c-myc expression and B cell lymphoma in mice

Rachel M. Gerstein; Charusheila Ramkumar; Yahui Kong; Hang Cui; Suyang Hao; Stephen N. Jones; Hong Zhang

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Hong Zhang

University of Massachusetts Medical School

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Yahui Kong

University of Massachusetts Medical School

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Charusheila Ramkumar

University of Massachusetts Medical School

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Rachel M. Gerstein

University of Massachusetts Medical School

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Stephen N. Jones

University of Massachusetts Medical School

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Anthony N. Imbalzano

University of Massachusetts Medical School

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Hong-Hong Zhang

University of Massachusetts Medical School

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Jeffrey A. Nickerson

University of Massachusetts Medical School

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Qiong Wu

University of Massachusetts Medical School

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Scott E. LeBlanc

University of Massachusetts Medical School

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