Search Results

You are looking at 1 - 2 of 2 items for

  • Author: Hua Gao x
  • Refine by access: All content x
Clear All Modify Search
Zhen-Xian Du
Search for other papers by Zhen-Xian Du in
Google Scholar
PubMed
Close
,
Ying Yan Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Ying Yan in
Google Scholar
PubMed
Close
,
Hai-Yan Zhang Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Hai-Yan Zhang in
Google Scholar
PubMed
Close
,
Bao-Qin Liu Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Bao-Qin Liu in
Google Scholar
PubMed
Close
,
Yan-Yan Gao Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Yan-Yan Gao in
Google Scholar
PubMed
Close
,
Xiao-Fang Niu Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Xiao-Fang Niu in
Google Scholar
PubMed
Close
,
Yifu Guan Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Yifu Guan in
Google Scholar
PubMed
Close
,
Xin Meng Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Xin Meng in
Google Scholar
PubMed
Close
, and
Hua-Qin Wang Department of Endocrinology and Metabolism, Department of Radiotherapy, Department of Geriatrics, Department of Biochemistry and Molecular Biology, The First Affiliated Hospital, China Medical University, Shenyang 110001, People's Republic of China

Search for other papers by Hua-Qin Wang in
Google Scholar
PubMed
Close

Proteasome inhibitors represent a novel class of antitumor agents with pre-clinical and clinical evidence of activity against hematologic malignancies and solid tumors. However, emerging evidence indicates that antiapoptotic factors may also accumulate as a consequence of exposure to these drugs, thus it seems plausible that the activation of survival signaling cascades might compromise their antitumoral effects. Peroxiredoxins (PRDXs) are a family of thiol-containing peroxidases identified primarily by their ability to remove cellular hydroperoxides. The function of PRDX1 in particular has been implicated in regulating cell proliferation, differentiation, and apoptosis. Another important finding is that aberrant upregulation of PRDX1 has been discovered in various cancers. Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK) kinase kinase that is regulated under conditions of cellular stress. ASK1 phosphorylates c-Jun N-terminal kinase and p38 MAPK, and elicits an apoptotic response. ASK1 activity is regulated at multiple levels, one of which is through interaction with PRDX1. In this study, for the first time we report that upregulation of PRDX1 expression was found in thyroid cancer cells treated with proteasome inhibitors, and PRDX1 knockdown resulted in accelerated proteasome inhibitor-induced cell death. In addition, we demonstrated that ASK1 activity was implicated in the PRDX1-dependent response of thyroid cancer cells to proteasome inhibitor-mediated cell death.

Free access
Bin Li Department of Neurosurgery, Peking University People’s Hospital, Beijing, China

Search for other papers by Bin Li in
Google Scholar
PubMed
Close
,
Sida Zhao Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

Search for other papers by Sida Zhao in
Google Scholar
PubMed
Close
,
Yiyuan Chen Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

Search for other papers by Yiyuan Chen in
Google Scholar
PubMed
Close
,
Hua Gao Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

Search for other papers by Hua Gao in
Google Scholar
PubMed
Close
,
Weiyan Xie Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

Search for other papers by Weiyan Xie in
Google Scholar
PubMed
Close
,
Hongyun Wang Department of Cell and Biology, Beijing Neurosurgical Institute, Capital Medical University, Beijing, China

Search for other papers by Hongyun Wang in
Google Scholar
PubMed
Close
,
Peng Zhao Department of Neurosurgical, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

Search for other papers by Peng Zhao in
Google Scholar
PubMed
Close
,
Chuzhong Li Department of Neurosurgical, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

Search for other papers by Chuzhong Li in
Google Scholar
PubMed
Close
, and
Yazhuo Zhang Department of Neurosurgical, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

Search for other papers by Yazhuo Zhang in
Google Scholar
PubMed
Close

The clinical diagnosis and treatment of pituitary neuroendocrine tumors (PitNETs) that invade the cavernous sinus are fraught with difficulties and challenges. Exploring the biological characteristics involved in the occurrence and development of PitNETs that invade the cavernous sinus will help to elucidate the mechanism of cavernous sinus invasion. There are differences between intrasellar tumors (IST) and cavernous sinus-invasion tumors (CST) in ultramicrostructure, tumor microenvironment (TME), gene expression, and signaling pathways. The microvascular endothelial cell is increased in CST. The VEGFR signaling pathway, VEGF signaling pathway, and chemokine signaling pathway are activated in CST. HSPB1 is upregulated in CST and promotes cell proliferation, cell viability, and migration. HSPB1 promotes the release of VEGF from GT1-1 cells and activates the VEGF signaling pathway in bEnd.3 cells. HSPB1 promotes the migration of bEnd.3 cells to GT1-1 cells and promotes the formation of blood vessels of bEnd.3 cells. bEnd.3 cells can release CCL3 and CCL4 and promote the vitality, proliferation, and migration of GT1-1 cells. HSPB1 promotes the formation of blood vessels of bEnd.3 cells and ultimately leads to tumor growth in vivo. HSPB1 acts as a key gene for invasion of the cavernous sinus in PitNETs, remodeling TME by promoting the formation of blood vessels of brain microvascular endothelial cells. The synergistic effect of tumor cells and microvascular endothelial cells promotes tumor progression. The mechanism by which HSPB1 promotes tumor invasion by inducing angiogenesis in PitNETs may be a new target for the treatment of PitNETs invading the cavernous sinus.

Restricted access