Overexpression of BST2 is associated with nodal metastasis and poorer prognosis in oral cavity cancer

Fang, Ku‐Hao; Kao, Huang‐Kai; Chi, Lang‐Ming; Li, Ying; Liu, Shiau-Chin; Hseuh, Chuen; Liao, Chun‐Ta; Yen, Tzu‐Chen; Yu, Jau‐Song; Chang, Kai‐Ping

doi:10.1002/lary.24700

Cited by 48 publications

(46 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…17, 36, 37 BST2 is also reported to promote the growth and metastasis of breast cancer. 16, 38 Thus, BST2 may have a proto-oncogenic role and promotes cancer progression, 38 which is also consistant with our observation that knockdown of BST2 delayed the growth of NPC xenografts in nude mice.…”

Section: Discussionmentioning

confidence: 99%

“…10, 11, 12 However, BST2 was first identified as a type II transmembrane glycoprotein expressed in bone marrow stromal cell lines and involved in pre-B-cell growth. 13 Accumulating evidence has shown that BST2 is also constitutively expressed on various other immune cells and malignant cells, 14, 15 such as breast cancer, 16 oral cavity cancer, 17 lung cancer, 18 B-cell chronic lymphocytic leukemia 19 and gastrointestinal cancer cells. 20 Nonetheless, BST2 is not elevated in all cancers.…”

mentioning

confidence: 99%

See 1 more Smart Citation

BST2 confers cisplatin resistance via NF-κB signaling in nasopharyngeal cancer

Kuang

Hua

et al. 2017

Cell Death Dis

View full text Add to dashboard Cite

Concurrent/adjuvant cisplatin-based chemoradiotherapy is regarded as the standard of treatment for locoregionally advanced nasopharyngeal carcinoma (NPC). However, patients who do not respond to cisplatin suffer, rather than benefit, from chemotherapy treatment. The goal of this study was to identify molecules involved in cisplatin resistance and to clarify their molecular mechanisms, which would help in the discovery of potential therapeutic targets and in developing a personalized and precise treatment approach for NPC patients. We previously generated a cisplatin-sensitive NPC cell line, S16, from CNE2 cells and found that eIF3a, ASNS and MMP19 are upregulated in S16 cells, which contributes to their cisplatin sensitivity. In this study, we found that BST2 is downregulated in cisplatin-sensitive S16 cells compared with CNE2 cells. Knockdown of BST2 in NPC cells sensitized their response to cisplatin and promoted cisplatin-induced apoptosis, whereas exogenous overexpression of BST2 increased their cisplatin resistance and inhibited cisplatin-induced apoptosis. Further investigation demonstrated that BST2-mediated cisplatin resistance depended on the activation of the NF-κB signaling pathway and consequent upregulation of anti-apoptotic genes, such as Bcl-XL and livin. Moreover, an analysis of clinical data revealed that a high BST2 level might serve as an independent indicator of poor prognosis in patients with locally advanced NPC treated with platinum-based chemoradiotherapy. These findings suggest that BST2 likely mediates platinum resistance in NPC, offering guidance for personalized and precise treatment strategies for patients with NPC.

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

BST2 confers cisplatin resistance via NF-κB signaling in nasopharyngeal cancer

Kuang

Hua

et al. 2017

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…The spectrum of BST-2 expression in various cancers has been revealed using meta analyses studies of large tumor datasets [119]. In solid tumors, BST-2 expression is elevated in head and neck cancer [120], lung cancer [121], breast cancer [119,122,123], cervical cancer [124], myelomas [125,126], endometrial cancer [127], and glioblastoma [128]. In addition, data from proteinatlas.org reveal that BST-2 is overexpressed in colorectal cancer, ovarian cancer, thyroid cancer, and pancreatic cancer (http://www.proteinatlas.org/ ENSG00000130303-BST2/cancer).…”

Section: Bst-2/tetherin: Roles In Carcinogenesismentioning

confidence: 99%

“…Correlation studies using meta analyses of various tumor datasets showed that BST-2 levels are proportional to the aggressiveness of different cancers including breast [123,129], brain [128], and oral cavity cancers [120]. In vitro, overexpression of BST-2 in breast cancer cells enhanced cell migration, invasion, proliferation, and anchorage-independent growth [119,123,129] whereas BST-2 suppression results in reduced migration, invasion, anchorage-independent growth but not cell proliferation [45].…”

Section: Functional Roles Of Bst-2 In Cancermentioning

confidence: 99%

The role of BST‐2/Tetherin in host protection and disease manifestation

Mahauad‐Fernandez

Okeoma

2015

Immunity, Inflammation and Disease

View full text Add to dashboard Cite

Host cells respond to viral infections by activating immune response genes that are not only involved in inflammation, but may also predispose cells to cancerous transformation. One such gene is BST‐2, a type II transmembrane protein with a unique topology that endows it tethering and signaling potential. Through this ability to tether and signal, BST‐2 regulates host response to viral infection either by inhibiting release of nascent viral particles or in some models inhibiting viral dissemination. However, despite its antiviral functions, BST‐2 is involved in disease manifestation, a function linked to the ability of BST‐2 to promote cell‐to‐cell interaction. Therefore, modulating BST‐2 expression and/or activity has the potential to influence course of disease.

show abstract

“…Although BST-2 is thought to antagonize the release of host cells from enveloped viruses, recent studies have shown that BST-2 is highly expressed in many types of tumors, such as head and neck tumors [7] , lung cancer [8], and breast cancer. [6,9] , cervical cancer [10] , myeloma, endometrial cancer [11] , etc., suggesting that BST-2 has a carcinogenic effect.…”

Section: Discussionmentioning

confidence: 99%