Sanggenon O induced apoptosis of A549 cells is counterbalanced by protective autophagy

Li, Zhongrui; Ma, Ting; Guo, Yan-Jia; Hu, Bo; Niu, Sheng-Hui; Suo, Feng-Zhi; Du, Linna; You, Yinghua; Kang, Wen-Ting; Shuan, Liu; Mamun, M. A. A.; Song, Qimeng; Pang, Jing-Ru; Zheng, Yi-Chao; Liu, Hong‐Min

doi:10.1016/j.bioorg.2019.03.072

Cited by 5 publications

(4 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This process is tightly regulated by Bcl-2 family proteins, which function in the mitochondrial membrane. 29 According to our study, rapamycin decreased the P. aeruginosa-induced expression of the caspase-9, Bax and cytc proteins, but increased the expression of Bcl-2. Furthermore, the activation of mitochondrial apoptosis was also associated with a change in MMP.…”

Section: Discussionmentioning

confidence: 54%

Autophagy plays a protective role duringPseudomonas aeruginosa-induced apoptosis via ROS–MAPK pathway

Han

et al. 2020

Innate Immun

View full text Add to dashboard Cite

Pseudomonas aeruginosa infection can induce alveolar macrophage apoptosis and autophagy, which play a vital role in eliminating pathogens. These two processes are usually not independent. Recently, autophagy has been found to interact with apoptosis during pathogen infections. Nevertheless, the role of autophagy in P. aeruginosa-infected cell apoptosis is unclear. In this study, we explored the impact of P. aeruginosa infection on autophagy and apoptosis in RAW264.7 cells. The autophagy activator rapamycin was used to stimulate autophagy and explore the role of autophagy on apoptosis in P. aeruginosa-infected RAW264.7 cells. The results indicated that P. aeruginosa infection induced autophagy and apoptosis in RAW264.7 cells, and that rapamycin could suppress P. aeruginosa-induced apoptosis by regulating the expression of apoptosis-related proteins. In addition, rapamycin scavenged the cellular reactive oxygen species (ROS) and diminished p-JNK, p-ERK1/2 and p-p38 expression of MAPK pathways in RAW264.7 cells infected with P. aeruginosa. In conclusion, the promotion of autophagy decreased P. aeruginosa-induced ROS accumulation and further attenuated the apoptosis of RAW264.7 cells through MAPK pathway. These results provide novel insights into host–pathogen interactions and highlight a potential role of autophagy in eliminating P. aeruginosa.

show abstract

Section: Discussionmentioning

confidence: 54%

Autophagy plays a protective role duringPseudomonas aeruginosa-induced apoptosis via ROS–MAPK pathway

Han

et al. 2020

Innate Immun

View full text Add to dashboard Cite

show abstract

“…On the other hand, thiophene and its analogs [ 11 ] show interesting properties in medicinal chemistry, especially in cancer. In addition, many DA adducts are known for their antitumoral effects [ 12 , 13 ]. The synthetic drawbacks for obtaining thiophene DA adducts have been limited to a few biological studies [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

New Experimental Conditions for Diels–Alder and Friedel-Crafts Alquilation Reactions with Thiophene: A New Selenocyanate with Potent Activity against Cancer

2022

View full text Add to dashboard Cite

The reactivity of thiophene in Diels-Alder reactions is investigated with different maleimide derivatives. In this paper, we have synthesized for the first time the Diels–Alder adducts of thiophene at room temperature and atmospheric pressure. Maleimido–thiophene adducts were promoted by AlCl3. The effects of solvent, time, temperature and the use of different Lewis acids were studied, showing dramatic effects for solvent and Lewis acid. Furthermore, the catalysis with AlCl3 is highly stereoselective, preferably providing the exo form of the adduct. Additionally, we also discovered the ability of AlCl3 to catalyze the arylation of maleimides to yield 3-aryl succinimides in a straightforward manner following a Friedel–Crafts-type addition. The inclusion of a selenocyanate group contributes to the cytotoxic activity of the adduct. This derivatization (from compound 7 to compound 15) results in an average GI50 value of 1.98 µM in the DTP (NCI-60) cell panel, resulting in being especially active in renal cancer cells.

show abstract

“…oreS has also been observed to exert strong neuroprotective effects, as it reduces neuronal oxidative damage (32,33). notably, oreS and its derivatives have been reported to serve an efficient role against various types of cancer, such as head and neck carcinoma (28), neuroblastoma (29), prostate (30), kidney (34) and lung cancer (35). However, it remains unknown whether ORES has an effect on the inhibition of osteosarcoma cells and the mechanism by which oreS inhibits tumor cell viability.…”

Section: Introductionmentioning

confidence: 99%

Oxyresveratrol induces apoptosis and inhibits cell viability via inhibition of the STAT3 signaling pathway in Saos‑2 cells

Jian

et al. 2020

Mol Med Rep

View full text Add to dashboard Cite

oxyresveratrol (oreS) is a natural phenolic compound with multiple biological functions including antioxidation, anti-inflammation and neuroprotection; however, the inhibitory effect of oreS on osteosarcoma remains largely unknown. The present study aimed to determine the effects of oreS on osteosarcoma cell Saos-2. cell counting Kit-8 assay was performed to detect Soas-2 cell viability. annexin-FiTc/Pi staining and Jc-1 staining were used to measure cell apoptosis and the change of mitochondrial membrane potential. in addition, western blotting was conducted to determine the expression levels of apoptotic proteins and the phosphorylation of STaT3. it was found that oreS inhibited cell viability and induced apoptosis of osteosarcoma Saos-2 cells in a concentration-dependent manner. in addition, oreS increased the expression levels of apoptotic proteases caspase-9 and caspase-3 and reduced mitochondrial membrane potential. in response to oreS treatment, the expression levels of pro-apoptotic proteins, Bad and Bax, were enhanced, whereas those of anti-apoptotic proteins, Bcl-2 and Bcl-xl, were reduced. in addition, the phosphorylation of STaT3 was attenuated in Saos-2 cells after treatment with oreS. inhibition of cell viability and apoptosis induction by oreS were rescued by enhancement of STaT3 activation upon treatment with il-6. collectively, the present study indicated that oreS induced apoptosis and inhibited cell viability, which may be associated with the inhibition of STAT3 activation; thus, ORES represents a promising agent for treating osteosarcoma.

show abstract

Sanggenon O induced apoptosis of A549 cells is counterbalanced by protective autophagy

Cited by 5 publications

References 50 publications

Autophagy plays a protective role duringPseudomonas aeruginosa-induced apoptosis via ROS–MAPK pathway

Autophagy plays a protective role duringPseudomonas aeruginosa-induced apoptosis via ROS–MAPK pathway

New Experimental Conditions for Diels–Alder and Friedel-Crafts Alquilation Reactions with Thiophene: A New Selenocyanate with Potent Activity against Cancer

Oxyresveratrol induces apoptosis and inhibits cell viability via inhibition of the STAT3 signaling pathway in Saos‑2 cells

Contact Info

Product

Resources

About