Vanadium pentoxide increased PTEN and decreased SHP1 expression in NK-92MI cells, affecting PI3K-AKT-mTOR and Ras-MAPK pathways

Gallardo-Vera, Francisco; Tapia-Rodríguez, Miguel; Díaz, Daniel; Fortoul, Teresa I.; Montaño, Luis F.; Rendón-Huerta, Erika P.

doi:10.1080/1547691x.2017.1404662

Cited by 17 publications

(11 citation statements)

References 46 publications

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“…Toxicity of vanadium compounds increases as the valence does (Barceloux, ), and the main difference between vanadyl sulfate and sodium metavanadate is their valence (Mukherjee et al, ). Although vanadate induces TNFα secretion (Ye et al, ), VOSO 4 and NaVO 3 did not, similarly to the non‐inducing effect of vanadium pentoxide on the NK‐92MI‐treated cells (Gallardo‐Vera et al, ).…”

Section: Discussionmentioning

confidence: 93%

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Vanadium compounds and cellular death mechanisms in the A549 cell line: The relevance of the compound valence

Guerrero-Palomo

Rendón-Huerta

Montaño

et al. 2018

J of Applied Toxicology

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Non‐small lung cell carcinoma has a high morbidity and mortality rates. The elective treatment for stage III and IV is cisplatinum that conveys serious toxic side effects. Vanadium compounds are metal molecules with proven antitumor activity that depends on its valence. Therefore, a better understanding of the mechanism of action of vanadium compounds is required. The aim of our study was to investigate the mechanisms of cell death induced by sodium metavanadate (NaVO3 [V(+5)]) and vanadyl sulfate (VOSO4 [(+4)]), both of which have reported apoptotic‐inducing activity. We exposed the A549 cell line to various concentrations (0‐100 μM) and to different exposure times to each compound and determined the cell viability and expression of caspases, reactive oxygen species (ROS) production, Bcl2, Bax, FasL and NO. Our results showed that neither compounds modified the basal expression of caspases or pro‐ and anti‐apoptotic proteins. The only change observed was the 12‐ and 14‐fold significant increase in ROS production induced by NaVO3 and VOSO4, respectively, at 100 μm concentrations after 48 hours. Our results suggest that classical apoptotic mechanisms are not related to the cell death induced by the vanadium compounds evaluated here, and showed that the higher ROS production was induced by the [(+4)] valence compound. It is possible that the difference will be secondary to its higher oxidative status and thus higher ROS production, which leads to higher cell damage. In conclusion, our results suggest that the efficacy of the cell death mechanisms induced by vanadium compounds differ depending on the valence of the compound.

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Section: Discussionmentioning

confidence: 93%

“…Although vanadate induces TNFα secretion (Ye et al, 1999), VOSO 4 and NaVO 3 did not, similarly to the non-inducing effect of vanadium pentoxide on the NK-92MI-treated cells (Gallardo-Vera et al, 2018).…”

Section: Discussionmentioning

confidence: 95%

Vanadium compounds and cellular death mechanisms in the A549 cell line: The relevance of the compound valence

Guerrero-Palomo

Rendón-Huerta

Montaño

et al. 2018

J of Applied Toxicology

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“…mTOR/Akt is an important apoptosis pathway. 28 Increasing the activity of the NOTCH pathway can inhibit the activity of the mTOR/Akt pathway and promote apoptosis. 29 In our experiment, after bile sulfonic acid induced acute pancreatitis, the activity of the NOTCH pathway increased, the activity of mTOR/Akt was inhibited, and the activities of apoptosis proteins, including Fas, FasL, Bax, caspase-9, and caspase-3, increased in the intestinal tract.…”

Section: Discussionmentioning

confidence: 99%

Effects of emodin on intestinal mucosal barrier by the upregulation of miR-218a-5p expression in rats with acute necrotizing pancreatitis

Tan

Zhang

et al. 2020

Int J Immunopathol Pharmacol

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Emodin is an effective component in rhubarb to cure intestinal dysfunction, but the specific mechanism remains unknown. This study aimed to evaluate the protective effects of emodin on intestinal dysfunction caused by acute severe pancreatitis and reveal the functional mechanism of emodin in the treatment of this condition. An acute severe pancreatitis model was prepared using taurocholate. In the treatment group, 50 mg/kg emodin was injected intravenously 2 h before the induction of acute severe pancreatitis at an interval of 8 h. After 24 h, the gene expression and protein levels of miR-218a-5p, RhoA, ROCK1, Akt, Notch1, Bax, Bcl-2, Fas, FasL, caspase-3, and caspase-9 were determined through reverse transcription polymerase chain reaction and Western blot analysis. The protein levels of occludin, zonula occludens-1 (ZO-1), and E-cadherin in the intestinal tract were also determined through Western blot analysis. The effects of miR-218a-5p on the apoptosis of rat intestinal epithelial cell-18 were observed through flow cytometry. The effects of emodin on intestinal cell apoptosis induced by acute severe pancreatitis were observed via TUNEL (terminal deoxynucleotidyl transferase dUTP nick-end labeling). Pathological changes in the pancreas and intestine of rats in each group were observed through hematoxylin and eosin staining. After 24 h of acute severe pancreatitis induced by taurocholate, emodin reduced the expression of miR-218a-5p in the intestinal tract; increased the expression of Notch1 and Bcl-2; decreased the expression levels of RhoA, ROCK1, Akt, Bax, Fas, FasL, caspase-3, and caspase-9; inhibited the intestinal cell apoptosis caused by acute severe pancreatitis; increased the protein expression levels of occludin, zonula occludens-1 (ZO-1), and E-cadherin in the intestinal tract; and alleviated intestinal dysfunction caused by acute severe pancreatitis. Emodin could regulate Notch1 and RhoA/ROCK pathways by regulating the miR-218a-5p expression in the intestine. It could also inhibit intestinal cell apoptosis induced by acute severe pancreatitis and improve the intestinal dysfunction caused by severe acute pancreatitis.

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“…When phosphoinositol-dependent kinases (PDK)1 and PDK2 participate in the reaction, AKT is phosphorylated at Ser473 and Thr308, thereby activating and phosphorylating AKT to produce p-AKT, which results in various physiological effects. Activated p-AKT phosphorylates mTOR directly (21). Mammalian mTOR is a component of mechanistic target of rapamycin c1 (mTORc1).…”

Section: Discussionmentioning

confidence: 99%

Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway

Liu

Wang

et al. 2020

Int J Mol Med

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Autophagy is a lysosome-mediated cell contentdependent degradation pathway that leads to enhanced inflammation in an uncontrolled state. This study examined the role of autophagy in lipopolysaccharide (LPS)-induced brain inflammation and the effects of the traditional chinese medicine ligustrazine on LPS-induced neurocognitive impairment in rats. Furthermore, the molecular mechanisms by which ligustrazine influences neurocognitive impairments were explored. The production of the inflammatory mediators interleukin (IL)-1β and tumor necrosis factor (TNF)-α was analyzed using ELISAs, and the expression levels of the autophagy marker microtubule-associated protein light chain 3 (Lc3) II/I were analyzed using western blotting. LPS exposure upregulated the expression of IL-1β and TNF-α and downregulated the expression of Lc3 II/I. Ligustrazine activated autophagy by preventing the expression of phosphoinositide 3-kinase (PI3K), phosphorylated protein kinase B (p-AKT), and phosphorylated mammalian target of rapamycin (p-mTOR). The present results suggest that ligustrazine improved LPS-induced neurocognitive impairments by activating autophagy and ameliorated neuronal injury by regulating the PI3K/AKT/mTOR signaling pathway. These findings provide an important reference for the prevention and treatment of neuroinflammation.

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Vanadium pentoxide increased PTEN and decreased SHP1 expression in NK-92MI cells, affecting PI3K-AKT-mTOR and Ras-MAPK pathways

Abstract: ARTICLE HISTORY

Cited by 17 publications

References 46 publications

Vanadium compounds and cellular death mechanisms in the A549 cell line: The relevance of the compound valence

Vanadium compounds and cellular death mechanisms in the A549 cell line: The relevance of the compound valence

Effects of emodin on intestinal mucosal barrier by the upregulation of miR-218a-5p expression in rats with acute necrotizing pancreatitis

Ligustrazine ameliorates lipopolysaccharide‑induced neurocognitive impairment by activating autophagy via the PI3K/AKT/mTOR pathway

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