scholarly journals Combination of apoptin with photodynamic therapy induces nasopharyngeal carcinoma cell death in vitro and in vivo

2012 ◽  
Vol 28 (6) ◽  
pp. 2077-2082 ◽  
Author(s):  
XIAOYONG FANG ◽  
PING WU ◽  
JINYUN LI ◽  
LIN QI ◽  
YAOYUN TANG ◽  
...  
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cell ◽  
Nasopharyngeal Carcinoma Cell

Knockdown of annexin VII enhances nasopharyngeal carcinoma cell radiosensitivity in vivo and in vitro

2020 ◽  
Vol 28 (2) ◽  
pp. 129-139
Author(s):  
Si-Jie Gui ◽  
Ru-Lei Ding ◽  
Yan-Ping Wan ◽  
Li Zhou ◽  
Xu-Jun Chen ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cell ◽  
Nasopharyngeal Carcinoma Cell

Down-regulation of GnT-V inhibits nasopharyngeal carcinoma cell CNE-2 malignancy in vitro and in vivo

2011 ◽  
Vol 309 (2) ◽  
pp. 151-161 ◽  
Author(s):  
Ting Wei ◽  
Yahui Li ◽  
Enqing Zhuo ◽  
Weiliang Zhu ◽  
Hui Meng ◽  
...  
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cell ◽  
Down Regulation ◽  
Nasopharyngeal Carcinoma Cell

Adenovirus-mediated transfer of tris-shRNAs induced apoptosis of nasopharyngeal carcinoma cell in vitro and in vivo

2011 ◽  
Vol 309 (2) ◽  
pp. 162-169 ◽  
Author(s):  
Ji-Bo Han ◽  
Ze-Zhang Tao ◽  
Shi-Ming Chen ◽  
Yong-Gang Kong ◽  
Bo-Kui Xiao
Keyword(s):  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cell ◽  
Nasopharyngeal Carcinoma Cell ◽  
Induced Apoptosis

scholarly journals Indole-3-carbinol inhibits nasopharyngeal carcinoma cell growth in vivo and in vitro through inhibition of the PI3K/Akt pathway

2014 ◽  
Vol 8 (1) ◽  
pp. 207-212 ◽  
Author(s):  
CHENG-GANG MAO ◽  
ZE-ZHANG TAO ◽  
ZHE CHEN ◽  
CHEN CHEN ◽  
SHI-MING CHEN ◽  
...  
Keyword(s):  
Cell Growth ◽  
Nasopharyngeal Carcinoma ◽  
Carcinoma Cell ◽  
Akt Pathway ◽  
Nasopharyngeal Carcinoma Cell

scholarly journals Therapeutic evaluation of palbociclib and its compatibility with other chemotherapies for primary and recurrent nasopharyngeal carcinoma

2020 ◽  
Author(s):  
zhichao xue ◽  
Vivian Wai Yan Lui ◽  
Yongshu Li ◽  
Jia Lin ◽  
Chanping You ◽  
...  
Keyword(s):  
Cell Death ◽  
Nasopharyngeal Carcinoma ◽  
Cell Lines ◽  
Chemotherapeutic Drugs ◽  
Induce Cell Cycle Arrest ◽  
Ki 67 ◽  
Concurrent Treatment ◽  
Xenograft Models

Abstract Background: Recent genomic analyses revealed that druggable molecule targets were detectable in approximately 6% of patients with nasopharyngeal carcinoma (NPC). However, a dependency on dysregulated CDK4/6–cyclinD1 pathway signaling is an essential event in the pathogenesis of NPC. In this study, we aimed to evaluate the therapeutic efficacy of a specific CDK4/6 inhibitor, palbociclib, and its compatibility with other chemotherapeutic drugs for the treatment of NPC by using newly established xenograft models and cell lines derived from primary, recurrent, and metastatic NPC. Methods: We evaluated the efficacies of palbociclib monotherapy and concurrent treatment with palbociclib and cisplatin or suberanilohydroxamic acid (SAHA) in NPC cell lines and xenograft models. RNA sequencing was then used to profile the drug response–related pathways. Palbociclib-resistant NPC cell lines were established to determine the potential use of cisplatin as a second-line treatment after the development of palbociclib resistance. We further examined the efficacy of palbociclib treatment against cisplatin-resistant NPC cells. Results: In NPC cells, palbociclib monotherapy was confirmed to induce cell cycle arrest in the G1 phase in vitro . Palbociclib monotherapy also had significant inhibitory effects in all six tested NPC tumor models in vivo , as indicated by substantial reductions in the total tumor volumes and in Ki-67 proliferation marker expression. In NPC cells, concurrent palbociclib treatment mitigated the cytotoxic effect of cisplatin in vitro . Notably, concurrent treatment with palbociclib and SAHA synergistically promoted NPC cell death both in vitro and in vivo . This combination also further inhibited tumor growth by inducing autophagy-associated cell death. NPC cell lines with induced palbociclib or cisplatin resistance remained sensitive to treatment with cisplatin or palbociclib, respectively. Conclusions: Our study findings provide essential support for the use of palbociclib as an alternative therapy for NPC and increase awareness of the effective timing of palbociclib administration with other chemotherapeutic drugs. Our results provide a foundation for the design of first-in-human clinical trials of palbociclib regimens in patients with NPC.

Preclinical photodynamic therapy research in Spain 3: Localization of photosensitizers and mechanisms of cell deathin vitro

2009 ◽  
Vol 13 (04n05) ◽  
pp. 544-551 ◽  
Author(s):  
Magdalena Cañete ◽  
Juan C. Stockert ◽  
Angeles Villanueva
Keyword(s):  
Cell Death ◽  
Photodynamic Therapy ◽  
Cell Cultures ◽  
Cellular Localization ◽  
Cell Damage ◽  
Therapeutic Modality ◽  
Action Mechanisms ◽  
Cell Death Mechanisms

Photodynamic therapy (PDT) is a subject of increasing biomedical research and represents a very promising therapeutic modality for palliative or even curative treatment of some superficial or endoscopically accessible tumors. In addition to the first photosensitizers (PSs) applied (hematoporphyrin-based drugs), second generation PSs with improved photophysical and photobiological properties are now studied using cell cultures, experimental tumors and clinical trials. On the other hand, there is a growing interest in the analysis of cell death mechanisms by apoptosis, which is especially relevant in oncology, because many anticancer drugs work, at least in part, by triggering apoptosis in neoplastic cells both in vitro and in vivo. The evaluation of cell death mechanisms is an important parameter to determine the efficacy and the potential toxicity of a treatment, allowing better adjustment of protocol. Using cell cultures, our research team has studied the mechanisms of cell damage and death implicated in the photodynamic processes, as well as the relationship between the cellular localization of the PS and the organelle damage during photosensitization. The results obtained in our laboratory provide a deeper understanding on the action mechanisms that lead to cell inactivation by PDT, and also allow selection of PSs with higher potential for clinical application than those currently in use.

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