scholarly journals Anticancer Effects of Cyclocarya paliurus Polysaccharide (CPP) on Thyroid Carcinoma In Vitro and In Vivo

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Zhiwei He ◽  
Fangfang Lv ◽  
Yueli Gan ◽  
Jing Gu ◽  
Ting Que

In this study, we explored the role and mechanisms of Cyclocarya paliurus polysaccharide on cell apoptosis in thyroid cancer (TC) cells. The apoptosis of thyroid cancer cells in vitro and tumor tissues in vivo induced by Cyclocarya paliurus polysaccharide was determined by MTT assay and flow cytometric assay. The downstream molecules including phosphop-protein kinase B (p-Akt), Akt, B-cell lymphoma 2 (Bcl-2), and Bcl-2-associated X protein (Bax) in tumor tissue were evaluated by western blotting. MTT and flow cytometry assay in vitro revealed Cyclocarya paliurus polysaccharide-induced apoptosis of thyroid cancer cell line in a manner of time-dependent and dose-dependent. In vivo assay showed 50 mg/kg and 100 mg/kg Cyclocarya paliurus polysaccharide significantly suppressed the proliferation of thyroid cancer in mice. Western blotting showed downregulation of p-Akt, Akt, and Bcl-2 and upregulation of Bax. These results suggest that Cyclocarya paliurus polysaccharide may enhance thyroid cancer cell apoptosis by suppressing the activation of p-Akt, Akt, and Bcl-2 and activating Bax, which provide a novel use of CPP as a thyroid cancer treatment.

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yu Wang ◽  
Liming Zhu ◽  
Mei Guo ◽  
Gang Sun ◽  
Kun Zhou ◽  
...  

AbstractWHSC1 is a histone methyltransferase that facilitates histone H3 lysine 36 dimethylation (H3K36me2), which is a permissive mark associated with active transcription. In this study, we revealed how WHSC1 regulates tumorigenesis and chemosensitivity of colorectal cancer (CRC). Our data showed that WHSC1 as well as H3K36me2 were highly expressed in clinical CRC samples, and high WHSC1 expression is associated with poorer prognosis in CRC patients. WHSC1 reduction promoted colon cancer cell apoptosis both in vivo and in vitro. We found that B cell lymphoma-2 (BCL2) expression, an anti-apoptotic protein, is markedly decreased in after WHSC1 depletion. Mechanistic characterization indicated that WHSC1 directly binds to the promoter region of BCL2 gene and regulate its H3K36 dimethylation level. What’s more, our study indicated that WHSC1 depletion promotes chemosensitivity in CRC cells. Together, our results suggested that WHSC1 and H3K36me2 modification might be optimal therapeutic targets to disrupt CRC progression and WHSC1-targeted therapy might potentially overcome the resistance of chemotherapeutic agents.


2014 ◽  
Vol 21 (6) ◽  
pp. 865-877 ◽  
Author(s):  
Samantha K McCarty ◽  
Motoyasu Saji ◽  
Xiaoli Zhang ◽  
Christina M Knippler ◽  
Lawrence S Kirschner ◽  
...  

Increased p21-activated kinase (PAK) signaling and expression have been identified in the invasive fronts of aggressive papillary thyroid cancers (PTCs), including those withRET/PTC, BRAFV600E, and mutantRASexpression. Functionally, thyroid cancer cell motilityin vitrois dependent on group 1 PAKs, particularly PAK1. In this study, we hypothesize that BRAF, a central kinase in PTC tumorigenesis and invasion, regulates thyroid cancer cell motility in part through PAK activation. Using three well-characterized human thyroid cancer cell lines, we demonstrated in all cell lines thatBRAFknockdown reduced PAK phosphorylation of direct downstream targets. In contrast, inhibition of MEK activity either pharmacologically or with siRNA did not reduce PAK activity, indicating MEK is dispensable for PAK activity. Inhibition of cell migration through BRAF loss is rescued by overexpression of either constitutive active MEK1 or PAK1, demonstrating that both signaling pathways are involved in BRAF-regulated cell motility. To further characterize BRAF–PAK signaling, immunofluorescence and immunoprecipitation demonstrated that both exogenously overexpressed and endogenous PAK1 and BRAF co-localize and physically interact, and that this interaction was enhanced in mitosis. Finally, we demonstrated that acute induction of BRAFV600E expressionin vivoin murine thyroid glands results in increased PAK expression and activity confirming a positive signaling relationshipin vivo. In conclusion, we have identified a signaling pathway in thyroid cancer cells which BRAF activates and physically interacts with PAK and regulates cell motility.


2006 ◽  
Vol 12 (18) ◽  
pp. 5570-5577 ◽  
Author(s):  
Quang T. Luong ◽  
James O'Kelly ◽  
Glenn D. Braunstein ◽  
Jerome M. Hershman ◽  
H. Phillip Koeffler

2004 ◽  
pp. 557-564 ◽  
Author(s):  
JP Schroder-van der Elst ◽  
D van der Heide ◽  
JA Romijn ◽  
JW Smit

OBJECTIVE: Natural flavonoids (plant pigments) have been shown to inhibit thyroid peroxidase (TPO) in vitro and the growth of thyroid cancer cell lines. We have studied the role of flavonoids on the iodide transport and the growth of the human follicular thyroid cancer cell line (FTC133) which was stably transfected with the human Na(+)/I(-) symporter (hNIS). DESIGN AND METHODS: Cells were treated with flavonoids (0.5-50 microM) for 0, 2, 4 and 6 days; (125)I content and (125)I efflux of the cells and DNA content were measured. RESULTS: Cell growth was inhibited significantly at day 6 by most flavonoids. Eight out of ten flavonoids decreased the (125)I content of the cells at day 4. Morin did not influence the (125)I content of the cells and, surprisingly, myricetin increased the (125)I content of the cells. Kaempferol, apigenin, luteolin and F21388 decreased NIS mRNA expression after 15, 29 and 48 h; after 96 h NIS mRNA returned to normal. CONCLUSION: As TPO is not present in this cell line, the effects of the flavonoids on the iodide uptake are not related to organification. Myricetin was the only flavonoid studied that increased the influx and decreased the efflux of iodide. The effect of myricetin (decreased growth and increased retention of iodide) can be of therapeutic value in the radioiodide treatment of thyroid carcinoma.


2018 ◽  
Vol 119 (5) ◽  
pp. 4097-4102 ◽  
Author(s):  
Yan Jiang ◽  
Shuai Hao ◽  
Wuguo Tian ◽  
Bo Gao ◽  
Xiaohua Zhang ◽  
...  

2018 ◽  
Vol 18 (17) ◽  
pp. 1483-1493
Author(s):  
Ricardo Imbroisi Filho ◽  
Daniel T.G. Gonzaga ◽  
Thainá M. Demaria ◽  
João G.B. Leandro ◽  
Dora C.S. Costa ◽  
...  

Background: Cancer is a major cause of death worldwide, despite many different drugs available to treat the disease. This high mortality rate is largely due to the complexity of the disease, which results from several genetic and epigenetic changes. Therefore, researchers are constantly searching for novel drugs that can target different and multiple aspects of cancer. Experimental: After a screening, we selected one novel molecule, out of ninety-four triazole derivatives, that strongly affects the viability and proliferation of the human breast cancer cell line MCF-7, with minimal effects on non-cancer cells. The drug, named DAN94, induced a dose-dependent decrease in MCF-7 cells viability, with an IC50 of 3.2 ± 0.2 µM. Additionally, DAN94 interfered with mitochondria metabolism promoting reactive oxygen species production, triggering apoptosis and arresting the cancer cells on G1/G0 phase of cell cycle, inhibiting cell proliferation. These effects are not observed when the drug was tested in the non-cancer cell line MCF10A. Using a mouse model with xenograft tumor implants, the drug preventing tumor growth presented no toxicity for the animal and without altering biochemical markers of hepatic function. Results and Conclusion: The novel drug DAN94 is selective for cancer cells, targeting the mitochondrial metabolism, which culminates in the cancer cell death. In the end, DAN94 has been shown to be a promising drug for controlling breast cancer with minimal undesirable effects.


2021 ◽  
Vol 123 (3) ◽  
pp. 151700
Author(s):  
Marjan Ghorbani-Anarkooli ◽  
Sara Dabirian ◽  
Adib Zendedel ◽  
Hasan Moladoust ◽  
Mohammad hadi Bahadori

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