DOI . ORG {
}
Title[redir]:
HSK3486 Inhibits Colorectal Cancer Growth by Promoting Oxidative Stress and ATPase Inhibitory Factor 1 Activation | Digestive Diseases and Sciences
Description:
Background HSK3486 (ciprofol), a new candidate drug similar to propofol, exerts sedative and hypnotic effects through gamma-aminobutyric acid type A receptors; however, its potential role in colorectal cancer is currently unknown. Aims This study aimed to evaluate the effects of HSK3486 on colorectal cancer cell proliferation. Methods Imaging was performed to detect reactive oxygen species and mitochondrial membrane potential. Western blotting was used to determine the expression of target signals. The HSK3486 molecular mechanism was investigated through ATPase inhibitory factor 1 knockdown and xenograft model experiments to assess mitochondrial function in colorectal cancer cells. Results Cell Counting Kit-8 and Annexin V/propidium iodide double staining assays showed that HSK3486 inhibited colorectal cancer cell proliferation in a concentration-dependent manner. In addition, HSK3486 treatment increased the expression of B-cell lymphoma-2-associated X, cleaved caspase 3, and cleaved poly (ADP-ribose) polymerase, whereas myeloid cell leukemia-1 and B-cell lymphoma 2 expression decreased. HSK3486 promoted mitochondrial dysfunction by inducing ATPase inhibitor factor 1 expression. Furthermore, HSK3486 promoted oxidative stress, as shown by the increase in reactive oxygen species and lactate dehydrogenase levels, along with a decrease in mitochondrial membrane potential and ATP levels. ATPase inhibitor factor 1 small interfering RNA pretreatment dramatically increased the mitochondrial membrane potential and tumor size in a xenograft model following exposure to HSK3486. Conclusion Collectively, our findings revealed that HSK3486 induces oxidative stress, resulting in colorectal cancer cell apoptosis, making it a potential candidate therapeutic strategy for colorectal cancer.
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Keywords {π}
pubmed, article, google, scholar, cas, cancer, cell, central, sun, propofol, colorectal, cells, apoptosis, mitochondrial, hsk, chen, zhang, shanghai, stress, factor, induces, china, atpase, med, inhibitory, manuscript, nan, mol, sci, wang, authors, fudan, university, data, research, zhong, yue, zhou, miao, minli, ciprofol, potential, proliferation, expression, anesthesiology, biol, int, clinical, hospital, privacy,
Topics {βοΈ}
month download article/chapter patic ischemia/reperfusion injury mir-340/cdk2 signal axis nmdar-camkii-erk pathway gamma-aminobutyric acid type reactive oxygen species ros-mediated mechanism article digestive diseases mapk/erk signaling pathway nf-ΞΊb signaling central control point therapeutically leveraging gaba full article pdf promoting oxidative stress hsk3486 treatment increased regulating mir-124-3p national key research mir-24 signal pathway privacy choices/manage cookies hsk3486 molecular mechanism clinical research plan colorectal cancer cells b-cell lymphoma-2 colorectal cancer patient changhong miao candidate drug similar chemical molecule inhibitor propofol induces apoptosis mitochondrial permeability transition endoplasmic reticulum stress article nan breast cancer cells patients undergoing colonoscopy stem cell rep central implication published article cardia cancer cells propofol induces impairment holds exclusive rights mitochondrial membrane potential bladder cancer cells oncogenically transformed cells hepatocellular carcinoma cells human osteosarcoma cells inhibitor protein if1 myeloid cell leukemia-1 cell mol med trends cell biol cell cycle arrest european economic area
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headline:HSK3486 Inhibits Colorectal Cancer Growth by Promoting Oxidative Stress and ATPase Inhibitory Factor 1 Activation
description:HSK3486 (ciprofol), a new candidate drug similar to propofol, exerts sedative and hypnotic effects through gamma-aminobutyric acid type A receptors; however, its potential role in colorectal cancer is currently unknown. This study aimed to evaluate the effects of HSK3486 on colorectal cancer cell proliferation. Imaging was performed to detect reactive oxygen species and mitochondrial membrane potential. Western blotting was used to determine the expression of target signals. The HSK3486 molecular mechanism was investigated through ATPase inhibitory factor 1 knockdown and xenograft model experiments to assess mitochondrial function in colorectal cancer cells. Cell Counting Kit-8 and Annexin V/propidium iodide double staining assays showed that HSK3486 inhibited colorectal cancer cell proliferation in a concentration-dependent manner. In addition, HSK3486 treatment increased the expression of B-cell lymphoma-2-associated X, cleaved caspase 3, and cleaved poly (ADP-ribose) polymerase, whereas myeloid cell leukemia-1 and B-cell lymphoma 2 expression decreased. HSK3486 promoted mitochondrial dysfunction by inducing ATPase inhibitor factor 1 expression. Furthermore, HSK3486 promoted oxidative stress, as shown by the increase in reactive oxygen species and lactate dehydrogenase levels, along with a decrease in mitochondrial membrane potential and ATP levels. ATPase inhibitor factor 1 small interfering RNA pretreatment dramatically increased the mitochondrial membrane potential and tumor size in a xenograft model following exposure to HSK3486. Collectively, our findings revealed that HSK3486 induces oxidative stress, resulting in colorectal cancer cell apoptosis, making it a potential candidate therapeutic strategy for colorectal cancer.
datePublished:2024-02-20T00:00:00Z
dateModified:2024-02-20T00:00:00Z
pageStart:1214
pageEnd:1227
sameAs:https://doi.org/10.1007/s10620-023-08213-8
keywords:
Anesthesia
GABA receptor agonist
Apoptosis
ATPIF1
Colorectal cancer
Oxidative stress
Gastroenterology
Hepatology
Oncology
Transplant Surgery
Biochemistry
general
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headline:HSK3486 Inhibits Colorectal Cancer Growth by Promoting Oxidative Stress and ATPase Inhibitory Factor 1 Activation
description:HSK3486 (ciprofol), a new candidate drug similar to propofol, exerts sedative and hypnotic effects through gamma-aminobutyric acid type A receptors; however, its potential role in colorectal cancer is currently unknown. This study aimed to evaluate the effects of HSK3486 on colorectal cancer cell proliferation. Imaging was performed to detect reactive oxygen species and mitochondrial membrane potential. Western blotting was used to determine the expression of target signals. The HSK3486 molecular mechanism was investigated through ATPase inhibitory factor 1 knockdown and xenograft model experiments to assess mitochondrial function in colorectal cancer cells. Cell Counting Kit-8 and Annexin V/propidium iodide double staining assays showed that HSK3486 inhibited colorectal cancer cell proliferation in a concentration-dependent manner. In addition, HSK3486 treatment increased the expression of B-cell lymphoma-2-associated X, cleaved caspase 3, and cleaved poly (ADP-ribose) polymerase, whereas myeloid cell leukemia-1 and B-cell lymphoma 2 expression decreased. HSK3486 promoted mitochondrial dysfunction by inducing ATPase inhibitor factor 1 expression. Furthermore, HSK3486 promoted oxidative stress, as shown by the increase in reactive oxygen species and lactate dehydrogenase levels, along with a decrease in mitochondrial membrane potential and ATP levels. ATPase inhibitor factor 1 small interfering RNA pretreatment dramatically increased the mitochondrial membrane potential and tumor size in a xenograft model following exposure to HSK3486. Collectively, our findings revealed that HSK3486 induces oxidative stress, resulting in colorectal cancer cell apoptosis, making it a potential candidate therapeutic strategy for colorectal cancer.
datePublished:2024-02-20T00:00:00Z
dateModified:2024-02-20T00:00:00Z
pageStart:1214
pageEnd:1227
sameAs:https://doi.org/10.1007/s10620-023-08213-8
keywords:
Anesthesia
GABA receptor agonist
Apoptosis
ATPIF1
Colorectal cancer
Oxidative stress
Gastroenterology
Hepatology
Oncology
Transplant Surgery
Biochemistry
general
image:
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