Proteomic profiling between CNE‐2 and its strongly metastatic subclone S‐18 and functional characterization of HSP27 in metastasis of nasopharyngeal carcinoma

Li, Guo Ping; Wang, Hua; Lai, Yiu Kay; Chen, Shao Chun; Lin, Marie C.M.; Lü, Gang; Zhang, Jing Fang; He, Xiao; Qian, Chao Nan; Kung, Hsiang Fu

doi:10.1002/pmic.201000483

Cited by 22 publications

(14 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Two sets of cell lines, 5-8F (high tumorigenic and metastatic potential) and 6-10B (low tumorigenic and metastatic potential), which were derived from the NPC cell line SUNE-1 [21], and S18 (high tumorigenic and metastatic potential) and S26 (low tumorigenic and metastatic potential), which were derived from CNE-2 cells [22,23], represent good models for investigating the metastasis of NPC. For the first time, we compared these high metastatic potential and low metastatic potential cell lines (5-8F vs. 6-10B and S18 vs. S26) using microarrays to identify dysregulated lncRNAs that participate in NPC tumorigenesis.…”

Section: Introductionmentioning

confidence: 99%

Microarray Expression Profiling of Long Non-Coding RNAs Involved in Nasopharyngeal Carcinoma Metastasis

Wen

Tang

et al. 2016

IJMS

View full text Add to dashboard Cite

Increasing evidence has demonstrated a significant role for long non-coding RNAs (lncRNAs) in tumorigenesis. However, their functions in nasopharyngeal carcinoma (NPC) metastasis remain largely unknown. In this study, a model comparing high and low metastatic NPC cell lines (5-8F vs. 6-10B and S18 vs. S26) was constructed to determine the expression profile of lncRNAs using the microarray analysis, and we found 167 lncRNAs and 209 mRNAs were differentially expressed. Bioinformatic analysis indicated that the dysregulated mRNAs participated in important biological regulatory functions in NPC. Validation of 26 significantly dysregulated lncRNAs by qRT-PCR showed the expression patterns of 22 lncRNAs were in accordance with the microarray data. Furthermore, the expression level of ENST00000470135, which was the most upregulated lncRNA in high metastatic cell lines, was significantly higher in NPC cell lines and tissues with lymph node metastasis (LNM) and knocking down ENST00000470135 suppressed the migration, invasion and proliferation of NPC cells in vitro. In conclusion, our study revealed expression patterns of lncRNAs in NPC metastasis. The dysregulated lncRNAs may act as novel biomarkers and therapeutic targets for NPC.

show abstract

Section: Introductionmentioning

confidence: 99%

Microarray Expression Profiling of Long Non-Coding RNAs Involved in Nasopharyngeal Carcinoma Metastasis

Wen

Tang

et al. 2016

IJMS

View full text Add to dashboard Cite

show abstract

“…At present, the most important etiologic factors implicated in NPC pathogenesis are genetic aberrations, Epstein-Barr viral infection and chemical carcinogen exposure. The aberrantly expressed genes induced by these factors have been shown to play an important role in the development and progression of NPC [1][2][3][4][5][6][7][8]. However, the molecular mechanisms of NPC are not still fully understood.…”

Section: Introductionmentioning

confidence: 99%

Proteomic features of potential tumor suppressor NESG1 in nasopharyngeal carcinoma

et al. 2012

View full text Add to dashboard Cite

We previously defined the recently revised NESG1 gene as a potential tumor suppressor in nasopharyngeal carcinoma (NPC). Here, we further used proteomics technology to globally examine NESG1-controlled proteins in NPC cells. Twenty-six proteins were found to be deregulated by NESG1 using proteomics analysis while enolase 1 (alpha) (ENO1), heat shock protein 90 kDa beta (Grp94), member 1 (HSP90B1), and cathepsin D (CTSD) proteins were differentially expressed by Western blot. Interestingly, a-enolase (ENO1), an overexpressed gene in NPC, was confirmed as a NESG1-regulated protein in NPC cells. Overexpressed ENO1 not only restored cell proliferation and cell-cycle progression, but also antagonized the regulation of NESG1 to cell-cycle regulators p21 and CCNA1 expression as well as induced the expression of C-Myc, pRB, and E2F1 in NESG1-ovexpressed NPC cells. Real-time PCR and immunohistochemistry analysis showed that NESG1 expression is negatively correlated with ENO1 expression in NPC tissues. Our observations suggest that ENO1 downregulation plays an important role in NESG1-induced growth inhibition of NPC cancer cells.

show abstract

“…In addition, HSP27 seems to promote metastasis formation through its effect on cytoskeletal components and to favor resistance to chemotherapeutic agents (Hino et al 2000 ;Katoh et al 2000 ;Li et al 2011 ). Choi et al showed that HSP27 expression was directly responsible for colorectal cancer cell resistance to the chemotherapeutic agent irinotecan.…”

Section: Hsp27: Favors Fibrosismentioning

confidence: 99%

Small Heat Shock Proteins and Fibrosis

Bellaye

Burgy

Colas

et al. 2015

Heat Shock Proteins

View full text Add to dashboard Cite

Small heat shock proteins (sHSP) are involved in many essential cellular mechanisms both in physiologic and pathologic conditions. HSP27 (HSPB1), αB-crystallin (HSPB5) and HSP20 (HSPB6), the most studied members, are stressinducible chaperones with an anti-aggregation function. They have been shown to inhibit apoptosis by interacting with proteins involved in programmed cell death such as cytochrome c or caspases, to have anti-oxidant properties and/or to modulate protein homeostasis by participating in the proteasomal degradation of specifi c proteins under stress conditions. Heat shock proteins accumulate in cancer cells and this overexpression is needed for the cancer cells' survival. Accordingly, the inhibition of heat shock proteins such as HSP27 is an emerging strategy in cancer therapy (already is in phase II clinical trials). Fibrogenesis and cancer share several properties as both pathologies are characterized by genetic alterations, uncontrolled cell proliferation, altered cell interaction and communication and tissue invasion.The current review will discuss the involvement of HSP27, αB-crystallin and HSP20 in the process of fi brogenesis and in established organ fi brosis. We will dissect the impact of their function inducing the recruitment of infl ammatory cells, the

show abstract

Proteomic profiling between CNE‐2 and its strongly metastatic subclone S‐18 and functional characterization of HSP27 in metastasis of nasopharyngeal carcinoma

Cited by 22 publications

References 43 publications

Microarray Expression Profiling of Long Non-Coding RNAs Involved in Nasopharyngeal Carcinoma Metastasis

Microarray Expression Profiling of Long Non-Coding RNAs Involved in Nasopharyngeal Carcinoma Metastasis

Proteomic features of potential tumor suppressor NESG1 in nasopharyngeal carcinoma

Small Heat Shock Proteins and Fibrosis

Contact Info

Product

Resources

About