Control of optical contrast using gold nanoshells for optical coherence tomography imaging of mouse xenograft tumor model in vivo

2009 ◽  
Vol 14 (5) ◽  
pp. 054015 ◽  
Author(s):  
James Chen Yong Kah ◽  
Malini Olivo ◽  
Tzu Hao Chow ◽  
Kin San Song ◽  
Karen Zhen Yu Koh ◽  
...  
2021 ◽  
Vol 12 ◽  
Author(s):  
Yangbo Li ◽  
Pengzhan He ◽  
Yinghui Liu ◽  
Mingming Qi ◽  
Weiguo Dong

Introduction: The gastrointestinal malignancy, gastric cancer (GC), has a high incidence worldwide. Cisplatin is a traditional chemotherapeutic drug that is generally applied to treat cancer; however, drug tolerance affects its efficacy. Sodium butyrate is an intestinal flora derivative that has general anti-cancer effects in vitro and in vivo via pro-apoptosis effects and can improve prognosis in combination with traditional chemotherapy drugs. The present study aimed to assess the effect of sodium butyrate combined with cisplatin on GC.Methods: A Cell Counting Kit-8 assay was used to assess the viability of GC cells in vitro. Hoechst 33,258 staining and Annexin V-Phycoerythrin/7-Aminoactinomycin D were used to qualitatively and quantitatively detect apoptosis in GC cells. Intracellular reactive oxygen species (ROS) measurement and a mitochondrial membrane potential (MMP) assay kit were used to qualitatively and quantitatively reflect the function of mitochondria in GC cells. Western blotting was used to verify the above experimental results. A nude mouse xenograft tumor model was used to evaluate the anti-tumor efficacity of sodium and cisplatin butyrate in vivo.Results: Cisplatin combined with sodium butyrate increased the apoptosis of GC cells. In the nude mouse xenograft tumor model, sodium butyrate in combination with cisplatin markedly inhibited the growth of the tumor more effectively than either single agent. The combination of sodium butyrate and cisplatin increased the intracellular ROS, decreased the MMP, and suppressed the invasion and migration abilities of GC cells. Western blotting verified that the combination of sodium butyrate and cisplatin remarkably enhanced the levels of mitochondrial apoptosis-related pathway proteins.Conclusion: Sodium butyrate, a histone acetylation inhibitor produced by intestinal flora fermentation, combined with cisplatin enhanced the apoptosis of GC cells through the mitochondrial apoptosis-related pathway, which might be considered as a therapeutic option for GC.


1998 ◽  
Vol 4 (7) ◽  
pp. 861-865 ◽  
Author(s):  
Stephan A. Boppart ◽  
Brett E. Bouma ◽  
Costas Pitris ◽  
James F. Southern ◽  
Mark E. Brezinski ◽  
...  

2014 ◽  
Vol 3 (1) ◽  
pp. 47-60 ◽  
Author(s):  
Reshmi Rajendran ◽  
Wei Huang ◽  
Annie Mei Yee Tang ◽  
Jie Ming Liang ◽  
Stephanie Choo ◽  
...  

2020 ◽  
Vol 245 (11) ◽  
pp. 925-932 ◽  
Author(s):  
Fang Chen ◽  
Xiaohui Wang ◽  
Shuang Fu ◽  
Shaokun Wang ◽  
Yu Fu ◽  
...  

The covalently closed circular RNA has recently been proposed as a pivotal player in tumorigenesis. In the current study, we found that circ-CDYL was notably elevated in multiple myeloma tissue and plasma samples and had good diagnostic and prognostic efficacy. Functional assays showed that circ-CDYL enhanced the viability and DNA synthesis of multiple myeloma cells and inhibited apoptosis. Mechanically, cytoplasmic circ-CDYL was co-localized with miR-1180, and circ-CDYL absorbed miR-1180 to upregulate yes-associated protein (YAP), thereby facilitating multiple myeloma progression. Importantly, we further confirmed the existence of this circ-CDYL/miR-1180/YAP regulatory axis in vivo by using the xenograft tumor model. Taken together, our data demonstrate that circ-CDYL is novel promoter of multiple myeloma, and targeting circ-CDYL and its associated network implicates the therapeutic possibility for multiple myeloma patients. Impact statement Multiple myeloma (MM) is an extremely complex and heterogeneous disease, and its pathogenesis is poorly understood. Here, we described an important MM-related circular RNA (circRNA), circ-CDYL. It was remarkably increased in both MM cells and plasma. Depletion of circ-CDYL evidently stunted MM growth. Circ-CDYL could absorb miR-1180 and alleviated the repression of miR-1180 on YAP, leading to increased YAP expression, ultimately triggering MM uncontrolled growth. Therefore, our findings advance the understanding of MM pathogenesis, and also raise the possibility of considering circ-CDYL as a potential therapeutic intervention for MM.


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