Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma

10.3390/cancers10110427

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Main Authors: Lee, J.H, Kim, C, Lee, S.-G, Sethi, G, Ahn, K.S
Other Authors: DEPT OF PHARMACOLOGY
Format: Article
Published: 2020
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Online Access:https://scholarbank.nus.edu.sg/handle/10635/177833
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spelling sg-nus-scholar.10635-1778332020-10-20T13:55:52Z Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma Lee, J.H Kim, C Lee, S.-G Sethi, G Ahn, K.S DEPT OF PHARMACOLOGY caspase glutathione glutathione disulfide glycoside ophiopogonin d STAT3 protein unclassified drug animal experiment animal model animal tissue antineoplastic activity apoptosis Article cancer inhibition controlled study drug effect drug inhibition drug mechanism enzyme activation female gene gene expression human human cell mouse non small cell lung cancer nonhuman oxidative stress signal transduction 10.3390/cancers10110427 Cancers 10 11 427 2020-10-20T03:29:58Z 2020-10-20T03:29:58Z 2018 Article Lee, J.H, Kim, C, Lee, S.-G, Sethi, G, Ahn, K.S (2018). Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma. Cancers 10 (11) : 427. ScholarBank@NUS Repository. https://doi.org/10.3390/cancers10110427 20726694 https://scholarbank.nus.edu.sg/handle/10635/177833 Attribution 4.0 International http://creativecommons.org/licenses/by/4.0/ Unpaywall 20201031
institution National University of Singapore
building NUS Library
continent Asia
country Singapore
Singapore
content_provider NUS Library
collection ScholarBank@NUS
topic caspase
glutathione
glutathione disulfide
glycoside
ophiopogonin d
STAT3 protein
unclassified drug
animal experiment
animal model
animal tissue
antineoplastic activity
apoptosis
Article
cancer inhibition
controlled study
drug effect
drug inhibition
drug mechanism
enzyme activation
female
gene
gene expression
human
human cell
mouse
non small cell lung cancer
nonhuman
oxidative stress
signal transduction
spellingShingle caspase
glutathione
glutathione disulfide
glycoside
ophiopogonin d
STAT3 protein
unclassified drug
animal experiment
animal model
animal tissue
antineoplastic activity
apoptosis
Article
cancer inhibition
controlled study
drug effect
drug inhibition
drug mechanism
enzyme activation
female
gene
gene expression
human
human cell
mouse
non small cell lung cancer
nonhuman
oxidative stress
signal transduction
Lee, J.H
Kim, C
Lee, S.-G
Sethi, G
Ahn, K.S
Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma
description 10.3390/cancers10110427
author2 DEPT OF PHARMACOLOGY
author_facet DEPT OF PHARMACOLOGY
Lee, J.H
Kim, C
Lee, S.-G
Sethi, G
Ahn, K.S
format Article
author Lee, J.H
Kim, C
Lee, S.-G
Sethi, G
Ahn, K.S
author_sort Lee, J.H
title Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma
title_short Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma
title_full Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma
title_fullStr Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma
title_full_unstemmed Ophiopogonin D, a steroidal glycoside abrogates STAT3 signaling cascade and exhibits anti-cancer activity by causing GSH/GSSG imbalance in lung carcinoma
title_sort ophiopogonin d, a steroidal glycoside abrogates stat3 signaling cascade and exhibits anti-cancer activity by causing gsh/gssg imbalance in lung carcinoma
publishDate 2020
url https://scholarbank.nus.edu.sg/handle/10635/177833
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