mRNA and protein dataset of autophagy markers (LC3 and p62) in several cell lines

Gómez-Sánchez, Rubén; Yakhine-Diop, Sokhna M. S.; Rodríguez-Arribas, Mario; Pedro, José Manuel Bravo-San; Martínez-Chacón, Guadalupe; Uribe-Carretero, Elisabet; Castro, Diana Clemente; Pizarro-Estrella, Elisa; Fuentes, José; González‐Polo, Rosa A.

doi:10.1016/j.dib.2016.02.085

Cited by 41 publications

(29 citation statements)

References 4 publications

(6 reference statements)

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“…The ubiquitin‐binding protein p62 is involved in lysosome‐ or proteasome‐dependent protein degradation during autophagy flux activation. A defect in the autophagy process or blockage of lysosomal degradation indicated autophagy flux inhibition, and this was indicated by increased p62 protein expression . CG treatment for 12 hours resulted in a dose‐dependent increase in LC3‐II, indicating autophagosome formation, and decrease in p62, suggesting that lysosomal degradation occurred.…”

Section: Resultsmentioning

confidence: 99%

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Cardiac glycoside sensitized hepatocellular carcinoma cells to TRAIL via ROS generation, p38MAPK, mitochondrial transition, and autophagy mediation

Rasheduzzaman

Yin

Park

2019

Molecular Carcinogenesis

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A major concern in the clinical application of tumor necrosis factor related apoptosis‐inducing ligand (TRAIL) in tumors is the development of resistance. Therefore, agents that can potentially restore TRAIL sensitivity are important therapeutic targets for cancer treatment. Herein, we evaluated lanatoside c and digoxin, both of which are widely used cardiac glycosides (CGs), for their ability to sensitize human hepatocellular carcinoma cells (Huh‐7 and HepG2) through TRAIL‐induced apoptosis. CGs functionalize TRAIL as shown by its effect on intracellular reactive oxygen species (ROS) generation, which damages mitochondrial integrity and thereby confers intrinsic apoptotic caspase cascade during combined treatment. Caspase activation is dependent on ROS as shown by the ability of CGs to generate ROS and the ROS‐N‐acetylcysteine (NAC) relationship, which inhibits apoptosis during cotreatment by preventing the formation of caspase‐8 and ‐3. Furthermore, CGs triggered p38MAPK phosphorylation and NAC pre‐exposure blocked p38MAPK phosphorylation, which demonstrated that p38MAPK was dependent upon ROS generation. Additionally, CGs were found to be potent inducers of AMPK‐mediated protective autophagy as pharmacological and genetic autophagy inhibition reached the higher threshold of TRAIL‐mediated apoptosis. Finally, CGs downregulated the expression of the antiapoptotic protein Bcl‐2 and increased the translocation of proapoptotic protein cytochrome c, thereby inducing apoptosis. Collectively, these results indicate that CGs potentiate the enhanced cytotoxic capacity to TRAIL through ROS generation, p38MAPK phosphorylation, cell survival protein downregulation, and protective autophagy inhibition.

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Section: Resultsmentioning

confidence: 99%

“…protein expression. 38 CG treatment for 12 hours resulted in a dosedependent increase in LC3-II, indicating autophagosome formation, and decrease in p62, suggesting that lysosomal degradation occurred.…”

Section: Cgs Led To Mitochondrial Dysfunction Via Antiapoptotic Bclmentioning

confidence: 99%

Cardiac glycoside sensitized hepatocellular carcinoma cells to TRAIL via ROS generation, p38MAPK, mitochondrial transition, and autophagy mediation

Rasheduzzaman

Yin

Park

2019

Molecular Carcinogenesis

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“…3ab) was essentially identical to the phenotype without the DM pre-treatment (Figure 2(a-b)), indicating the differentiation phenotype is independent of the proliferation phenotype. We also detected the expression levels of a caspase 3, a key apoptosis regulatory gene [94], and two key autophagy regulatory genes (LC3B and P62) [95] and found that FGF9 treatment did not alter their expression levels. This result indicated that FGF9 treatment did not alter C2C12 cell apoptosis and autophagy (Supplemental Figure 4).…”

Section: Discussionmentioning

confidence: 99%

Fibroblast growth factor 9 (FGF9) inhibits myogenic differentiation of C2C12 and human muscle cells

et al. 2019

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Osteoporosis and sarcopenia (osteosarcopenia (OS)) are twin-aging diseases. The biochemical crosstalk between muscle and bone seems to play a role in OS. We have previously shown that osteocytes produce soluble factors with beneficial effects on muscle and vice versa. Recently, enhanced FGF9 production was observed in the OmGFP66 osteogenic cell line. To test its role in myogenic differentiation, C2C12 myoblasts were treated with recombinant FGF9. FGF9 as low as 10 ng/mL inhibited myogenic differentiation, suggesting that FGF9 might be a potential inhibitory factor produced from bone cells with effects on muscle cells. FGF9 (10–50 ng/mL) significantly decreased mRNA expression of MyoG and Mhc while increasing the expression of Myostatin. Consistent with the phenotype, RT-qPCR array revealed that FGF9 (10 ng/mL) increased the expression of Icam1 while decreased the expression of Wnt1 and Wnt6 decreased, respectively. FGF9 decreased caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) of C2C12 myotubes and reduced the expression of genes (i.e. Cacna1s, RyR2, Naftc3) directly associated with intracellular Ca2+ homeostasis. Myogenic differentiation in human skeletal muscle cells was similarly inhibited by FGF9 but required higher doses of 200 ng/mL FGF9. FGF9 was also shown to stimulate C2C12 myoblast proliferation. FGF2 and the FGF9 subfamily members FGF16 and FGF20 also inhibited C2C12 myoblast differentiation and enhanced proliferation. Intriguingly, the differentiation inhibition was independent of proliferation enhancement. These findings suggest that FGF9 may modulate myogenesis via a complex signaling mechanism.

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“…E2 and PPT inhibited oleic acid-induced increase of p62/Sqstm1 mRNA. p62/Sqstm1 gene is a well-known autophagy marker (Gómez-Sánchez et al, 2016). Recent study showed that estrogen inhibits autophagy in endometrial cancer (Zhou et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Effects of estrogen on fatty-acid-induced cytotoxicity in mouse Neuro-2a neural cells

Ogawa

Kyoya

Kimura

et al. 2020

Fundam. Toxicol. Sci.

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The accumulation of free fatty acids induces lipotoxicity in neural cells. Estrogen, 17βestradiol (E2) protects against the damage of cells in various organs and tissues. However, the role of E2 on lipotoxicity in neural cells remains unclear. In this study, we investigated the effects of E2 on stearic acid (saturated fatty acid)-and oleic acid (unsaturated fatty acid)-induced cytotoxicity in retinoic acid-induced mouse neuroblastoma Neuro-2a differentiated into neural cells. Cell viability was evaluated by lactate dehydrogenase release from Neuro-2a neural cells. Stearic acid and oleic acids suppressed the cell viability in a dose-dependent manner. E2 prevented oleic acid-induced cytotoxicity but had no effect on stearic acid-induced cytotoxicity. ERα-selective agonist prevented cytotoxicity in Neuro-2a neural cells. In contrast, ERβ-selective agonist slightly significantly enhanced the cytotoxicity in the presence of oleic acid. Oleic acid, but not stearic acid, increased the mRNA level of p62/Sqstm1. E2 treatment statistically significantly, but slightly, enhanced the stearic acid-induced Bax expression. In contrast, E2 and ERαselective agonist inhibited the oleic acid-induced the p62/Sqstm1 expression. Our results suggested that fatty acids induced cytotoxicity in Neuro-2a neural cells, and estrogen prevented the oleic acid-induced cytotoxicity via ERα, but not ERβ. Further studies are needed to understand the role of ERβ in neuron injury under normal conditions.

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mRNA and protein dataset of autophagy markers (LC3 and p62) in several cell lines

Cited by 41 publications

References 4 publications

Cardiac glycoside sensitized hepatocellular carcinoma cells to TRAIL via ROS generation, p38MAPK, mitochondrial transition, and autophagy mediation

Cardiac glycoside sensitized hepatocellular carcinoma cells to TRAIL via ROS generation, p38MAPK, mitochondrial transition, and autophagy mediation

Fibroblast growth factor 9 (FGF9) inhibits myogenic differentiation of C2C12 and human muscle cells

Effects of estrogen on fatty-acid-induced cytotoxicity in mouse Neuro-2a neural cells

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