scholarly journals Preparation of nanoparticles of β-cyclodextrin-loaded scutellarein anti-tumor activity research by targeting integrin αvβ3

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jundong Wang ◽  
Tianhao Li ◽  
Chaochi Yue ◽  
Sen Zhong ◽  
Xiangdong Yang ◽  
...  

Abstract Background The problems associated with the poor water solubility of anticancer drugs are one of the most important challenges in achieving effective cancer therapy. The present study was designed to evaluate the effect of scutellarein on human colon cancer cells in vitro by using a target αvβ3 novel scutellarein (Scu)-loaded niosome nanoparticle (β-CD-CL-Scu-cRGD). Results β-CD-CL-Scu-cRGD has a diameter of 140.2 nm and zeta potential of − 11.3 mV with constant physicochemical stability. The MTT assay showed both Scu and β-CD-CL-Scu-cRGD caused a decrease in cell proliferation and viability of LoVo, but β-CD-CL-Scu-cRGD showed better activity in vitro. Colony formation assay and flow cytometry assay showed that β-CD-CL-Scu-cRGD has a better effect on cell proliferation and apoptosis. In vivo, animal experimental results showed that β-CD-CL-Scu-cRGD can significantly inhibit tumor growth, and the bodyweight of mice decreases during the treatment of scutellarein and its derivatives. β-CD-CL-Scu-cRGD could inhibit the protein levels of Ki67 and αvβ3, thereby inhibiting tumor growth. Conclusions Although further in vitro and in vivo studies are necessary, our results suggested that β-CD-CL-Scu-cRGD could be an outstanding carrier to deliver Scu for potential therapeutic approaches into colon cancer.

2021 ◽  
Author(s):  
JUNDONG WANG ◽  
TIANHAO LI ◽  
CHAOCHI YUE ◽  
SEN ZHONG ◽  
XIANGDONG YANG ◽  
...  

Abstract BackgroundThe problems associated with poor water solubility of anticancer drugs are one of the most important challenges in achieving effective cancer therapy. The present study was designed to evaluate the effect of Scutellarein on human colon cancer cells in vitro by using a target αvβ-3 novel Scutellarein (Scu)-loaded niosome nanoparticle (β-CD-CL-Scu-cRGD).Resultsβ-CD-CL-Scu-cRGD has a diameter of 140.2nm and a zeta potential of -11.3 mV with a constant physicochemical stability. The MTT assay showed both Scu and β-CD-CL-Scu-cRGD caused a decrease in cell proliferation and viability of HT29, but β-CD-CL-Scu-cRGD showed better activity in vitro. Colony formation assay and flow cytometry assay showed that β-CD-CL-Scu-cRGD has a better effect on cell proliferation and apoptosis.ConclusionsAlthough further in vivo studies are necessary, our results suggested that β-CD-CL-Scu-cRGD could be an outstanding carrier to deliver Scu for potential therapeutic approaches into colon cancer.


2021 ◽  
Author(s):  
JUNDONG WANG ◽  
TIANHAO LI ◽  
CHAOCHI YUE ◽  
SEN ZHONG ◽  
XIANGDONG YANG ◽  
...  

Abstract BackgroundThe problems associated with poor water solubility of anticancer drugs are one of the most important challenges in achieving effective cancer therapy. The present study was designed to evaluate the effect of Scutellarein on human colon cancer cells in vitro by using a target αvβ3 novel Scutellarein (Scu)-loaded niosome nanoparticle (β-CD-CL-Scu-cRGD).Resultsβ-CD-CL-Scu-cRGD has a diameter of 140.2nm and a zeta potential of -11.3 mV with a constant physicochemical stability. The MTT assay showed both Scu and β-CD-CL-Scu-cRGD caused a decrease in cell proliferation and viability of LoVo, but β-CD-CL-Scu-cRGD showed better activity in vitro. Colony formation assay and flow cytometry assay showed that β-CD-CL-Scu-cRGD has a better effect on cell proliferation and apoptosis.ConclusionsAlthough further in vitro and vivo studies are necessary, our results suggested that β-CD-CL-Scu-cRGD could be an outstanding carrier to deliver Scu for potential therapeutic approaches into colon cancer.


2010 ◽  
Vol 21 (6) ◽  
pp. 538-543 ◽  
Author(s):  
Chiu-Li Yeh ◽  
Man-Hui Pai ◽  
Cheng-Chung Li ◽  
Yu-Ling Tsai ◽  
Sung-Ling Yeh

PPAR Research ◽  
2007 ◽  
Vol 2007 ◽  
pp. 1-9 ◽  
Author(s):  
G. Martinasso ◽  
M. Oraldi ◽  
A. Trombetta ◽  
M. Maggiora ◽  
O. Bertetto ◽  
...  

PPAR involvement in cell growth was investigated “in vivo” and “in vitro” and was correlated with cell proliferation and apoptotic death. “In vivo” PPARγandαwere evaluated in colon cancer specimens and adjacent nonneoplastic colonic mucosa. PPARγincreased in most cancer specimens versus mucosa, with a decrease in c-Myc and in PCNA proteins, suggesting that colon cancer growth is due to increased cell survival rather than increased proliferation. The prevalence of survival over proliferation was confirmed by Bcl-2 or Bcl-XLincrease in cancer versus mucosa, and by decreased PPARα. “In vitro” PPARγand PPARαwere evaluated in human tumor and normal cell lines, treated with natural or synthetic ligands. PPARγwas involved in inhibiting cell proliferation with a decrease in c-Myc protein, whereas PPARαwas involved in inducing apoptosis with modulation of Bcl-2 and Bad proteins. This involvement was confirmed using specific antagonists of two PPARs. Moreover, the results obtained on treating cell lines with PPAR ligands confirm observations in colon cancer: there is an inverse correlation between PPARαand Bcl-2 and between PPARγand c-Myc.


2021 ◽  
Vol 14 (11) ◽  
pp. 1070
Author(s):  
Elena V. Lukasheva ◽  
Gulalek Babayeva ◽  
Saida Sh. Karshieva ◽  
Dmitry D. Zhdanov ◽  
Vadim S. Pokrovsky

L-lysine α-oxidase (LO), one of L-amino acid oxidases, deaminates L-lysine with the yield of H2O2, ammonia, and α-keto-ε-aminocaproate. Multiple in vitro and in vivo studies have reported cytotoxic, antitumor, antimetastatic, and antitumor activity of LO. Unlike asparaginase, LO has a dual mechanism of action: depletion of L-lysine and formation of H2O2, both targeting tumor growth. Prominent results were obtained on murine and human tumor models, including human colon cancer xenografts HCT 116, LS174T, and T47D with maximum T/C 12, 37, and 36%, respectively. The data obtained from human cancer xenografts in immunodeficient mice confirm the potential of LO as an agent for colon cancer treatment. In this review, we discuss recently discovered molecular mechanisms of biological action and the potential of LO as anticancer enzyme.


2002 ◽  
Vol 13 (5) ◽  
pp. 533-543 ◽  
Author(s):  
Jane-Jen Wang ◽  
Yaw-Terng Chern ◽  
Yuh-Fang Chang ◽  
Tsung-Yun Liu ◽  
Chin-Wen Chi

2019 ◽  
Vol 8 (12) ◽  
pp. 5662-5672 ◽  
Author(s):  
Sonoko Chikamatsu ◽  
Ken Saijo ◽  
Hiroo Imai ◽  
Koichi Narita ◽  
Yoshifumi Kawamura ◽  
...  

Author(s):  
Longgang Wang ◽  
Jinxiang Guo ◽  
Jin Zhou ◽  
Dongyang Wang ◽  
Xiuwen Kang ◽  
...  

Abstract Background Colon cancer represents one of the leading causes of gastrointestinal tumors in industrialized countries, and its incidence appears to be increasing at an alarming rate. Accumulating evidence has unveiled the contributory roles of cancer stem cells (CSCs) in tumorigenicity, recurrence, and metastases. The functions of NF-kappa B (NF-κB) activation on cancer cell survival, including colon cancer cells have encouraged us to study the role of NF-κB in the maintenance of CSCs in colon cancer. Methods Tumor samples and matched normal samples were obtained from 35 colon cancer cases. CSCs were isolated from human colon cancer cell lines, where the stemness of the cells was evaluated by cell viability, colony-forming, spheroid-forming, invasion, migration, and apoptosis assays. NF-κB activation was then performed in subcutaneous tumor models of CSCs by injecting lipopolysaccharides (LPS) i.p. Results We found that NF-κB activation could reduce the expression of miR-195-5p and miR-497-5p, where these two miRNAs were determined to be downregulated in colon cancer tissues, cultured colon CSCs, and LPS-injected subcutaneous tumor models. Elevation of miR-195-5p and miR-497-5p levels by their specific mimic could ablate the effects of NF-κB on the stemness of colon cancer cells in vivo and in vitro, suggesting that NF-κB could maintain the stemness of colon cancer cells by downregulating miR-195-5p/497–5p. MCM2 was validated as the target gene of miR-195-5p and miR-497-5p in cultured colon CSCs. Overexpression of MCM2 was shown to restore the stemness of colon cancer cells in the presence of miR-195-5p and miR-497-5p, suggesting that miR-195-5p and miR-497-5p could impair the stemness of colon cancer cells by targeting MCM2 in vivo and in vitro. Conclusions Our work demonstrates that the restoration of miR-195-5p and miR-497-5p may be a therapeutic strategy for colon cancer treatment in relation to NF-κB activation.


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