human colon cancer cells
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2021 ◽  
Vol 23 (2) ◽  
Author(s):  
Zheng Han ◽  
Liu Meng ◽  
Xiaodong Huang ◽  
Jie Tan ◽  
Weijie Liu ◽  
...  

Author(s):  
Yan Li ◽  
Hailong Lei ◽  
Ming Zhang ◽  
Guangming Wu ◽  
Caiyun Guo ◽  
...  

Background: To study the molecular mechanism of cisplatin chemotherapy resistance in colorectal cancer cells and to explore the effect of miRNA in regulating the expression of glucose transporter 3 (SLC2A3) and the proliferation and migration of colon cancer cells. Methods: All samples were obtained from the People’s Hospital of Wuhai, Wuhai, China between June 2019 and June 2020. Real-time quantitative PCR (qRT-PCR) was carried out to check the expression of miR-103a in these cell lines. Western blotting and Luciferase reporter gene detection confirmed the regulation of the miR-103a/SLC2A3 axis. Western blotting detected the activation of SLC2A3, caspased-9 and -3. Results: The expression of SLC2A3 protein in colon cancer cell lines was significantly higher than that of normal colon cancer cells, while the expression of SLC2A3 miRNA showed no significant difference (P<0.05). Then, through clone formation analysis, SLC2A3 was closely related to the proliferation of human colon cancer cells. Functional recovery experiments showed that increasing the expression of miR-103a could reverse the abnormal proliferation caused by overexpression of SLC2A3. Conclusion: Overall, miR-103a can inhibit the proliferation of human colon cancer cells by targeting SLC2A3, and this result will provide a potential target for the treatment of colon cancer.


2021 ◽  
Vol 220 (12) ◽  
Author(s):  
Kenta Tsuchiya ◽  
Gohta Goshima

The γ-tubulin complex acts as the predominant microtubule (MT) nucleator that initiates MT formation and is therefore an essential factor for cell proliferation. Nonetheless, cellular MTs are formed after experimental depletion of the γ-tubulin complex, suggesting that cells possess other factors that drive MT nucleation. Here, by combining gene knockout, auxin-inducible degron, RNA interference, MT depolymerization/regrowth assay, and live microscopy, we identified four microtubule-associated proteins (MAPs), ch-TOG, CLASP1, CAMSAPs, and TPX2, which are involved in γ-tubulin–independent MT generation in human colon cancer cells. In the mitotic MT regrowth assay, nucleated MTs organized noncentriolar MT organizing centers (ncMTOCs) in the absence of γ-tubulin. Depletion of CLASP1 or TPX2 substantially delayed ncMTOC formation, suggesting that these proteins might promote MT nucleation in the absence of γ-tubulin. In contrast, depletion of ch-TOG or CAMSAPs did not affect the timing of ncMTOC appearance. CLASP1 also accelerates γ-tubulin–independent MT regrowth during interphase. Thus, MT generation can be promoted by MAPs without the γ-tubulin template.


Biomedicines ◽  
2021 ◽  
Vol 9 (11) ◽  
pp. 1604
Author(s):  
Hee Young Yoo ◽  
So Yeon Park ◽  
Sun-Young Chang ◽  
So Hee Kim

Butyrates inhibit cell growth in colon cancer cells by inhibiting histone deacetylases. However, chronic exposure to butyrates induces butyrate resistance in colon cancer cells. The mechanism underlying the acquisition of resistance is not yet fully understood. Here, butyrate-resistant (BR) colon cancer cells were developed in HCT116, HT29, and SW480 human colon cancer cells and were confirmed by the increase in the inhibitory concentrations of cell growth by 50% (IC50) compared to their respective parental (PT) cells. Chronic exposure to butyrate induced autophagy via higher expression of Beclin-1 and LC3B-II. The AMP-activated protein kinase (AMPK) was downregulated along with the activation of Akt and mammalian target of rapamycin (mTOR) and decrease in acetyl-CoA carboxylase (ACC) in BR colon cancer cells compared to those in their respective PT cells. Activation of AMPK by AICAR treatment in BR colon cancer cells suppressed cell proliferation by inhibiting Akt and mTOR and activating ACC. Taken together, chronic exposure to butyrate increased butyrate resistance in human colon cancer by inducing protective autophagy through the downregulation of AMPK/ACC and activation of Akt/mTOR signaling. Activation of AMPK restored sensitivity to butyrate by the inhibition of Akt/mTOR, suggesting that AMPK could be a therapeutic target for BR colon cancers.


Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1757
Author(s):  
Krishnendu K. Roy ◽  
Jiamo Lu ◽  
James H. Doroshow

Recent studies suggest that of the molecules postulated to function as inhibitors of the NADPH oxidase family of enzymes iodonium analogs known to broadly interfere with flavin dehydrogenase function demonstrate mechanistic validity as NADPH oxidase poisons. In recent work, we have produced a series of novel iodonium compounds as putative inhibitors of these oxidases. To evaluate the potential utility of two novel molecules with favorable chemical properties, NSC 740104 and NSC 751140, we compared effects of these compounds to the two standard inhibitors of this class, diphenyleneiodonium and di-2-thienyliodonium, with respect to antiproliferative, cell cycle, and gene expression effects in human colon cancer cells that require the function of NADPH oxidase 1. Both new agents blocked NADPH oxidase-related reactive oxygen production, inhibited tumor cell proliferation, produced a G1/S block in cell cycle progression, and inhibited NADPH oxidase 1 expression at the mRNA and protein levels at low nM concentrations in a fashion similar to or better than the parent molecules. These studies suggest that NSC 740104 and NSC 751140 should be developed further as mechanistic tools to better understand the role of NADPH oxidase inhibition as an approach to the development of novel therapeutic agents for colon cancer.


Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 6056
Author(s):  
Joanna Wezgowiec ◽  
Marta Tsirigotis-Maniecka ◽  
Jolanta Saczko ◽  
Mieszko Wieckiewicz ◽  
Kazimiera A. Wilk

This study aimed to characterize the hydrogel micro- and macro-particles designed to deliver curcumin to human colon cancer cells (LoVo). Six series of vehicles based on sodium alginate (micro- and macro-particles, uncoated, coated with chitosan or gelatin) were synthesized. The uncoated microparticles were fabricated using an emulsion-based technique and the uncoated macroparticles with an extrusion technique, with both coupled with ionotropic gelation. The surface morphology of the particles was examined with scanning electron microscopy and the average size was measured. The encapsulation efficiency, moisture content, and swelling index were calculated. The release of curcumin from the particles was studied in an experiment simulating the conditions of the stomach, intestine, and colon. To evaluate the anticancer properties of such targeted drug delivery systems, the cytotoxicity of both curcumin-loaded and unloaded carriers to human colon cancer cells was assessed. The microparticles encapsulated much less of the payload than the macroparticles and released their content in a more prolonged manner. The unloaded carriers were not cytotoxic to LoVo cells, while the curcumin-loaded vehicles impaired their viability—more significantly after incubation with microparticles compared to macroparticles. Gelatin-coated or uncoated microparticles were the most promising carriers but their potential anticancer activity requires further thorough investigation.


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