CORRECTION article

Front. Pharmacol., 08 September 2023

Sec. Pharmacology of Anti-Cancer Drugs

Volume 14 - 2023 | https://doi.org/10.3389/fphar.2023.1274076

Corrigendum: Paraptosis: a unique cell death mode for targeting cancer

  • 1. School of Biotechnology, Amrita Vishwa Vidyapeetham, Kollam, Kerala, India

  • 2. Department of Cell Systems and Anatomy, UT Health San Antonio, San Antonio, TX, United States

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In the published article, there was an error in Table 3 as published. The cell line type and the signalling pathway and mechanism attributed to the article by Garrido-Armas et al. (2018) was incorrect. The corrected Table 3 appear below.

TABLE 3

Sl. No:CompoundsCell line typeCell lineSignalling pathway and mechanismReferences
1. Breast
i)CurcuminMelanocyteMDA-MB-434SInhibition of mitochondrial Na+/Ca2+ exchanger (mNCX) and proteasome, pERK1/2↑, p-JNKs↑, Alix↓Yoon et al. 2010 (2012)
EpithelialMDA-MB-231, HS578T
ii)Dimethoxy curcuminMelanocyteMDA-MB-434SProteasomal inhibition and ER stress, pERK1/2↑, p-JNKs ↑, Alix↓Yoon et al. (2014a)
EpithelialMDA-MB-231, HS578T, MCF-7
iii)CelastrolMelanocyteMDA-MB-434SCa2+ overload, proteasomal inhibition via ER stress, pERK1/2↑, p-JNKs ↑, p-p38Yoon et al. (2014)
EpithelialMCF-7
iv)15d-PGJ2EpithelialMDA-MB-231Disruption of sulfhydryl homeostasis, ER stress, pERK1/2↑Kar et al. (2009)
v)Manumycin AEpithelialMDA-MB-231, BT-20ER stress, accumulation of ubiquitinated proteins, p21↑, p27 ↑, PTEN ↑Singha et al. (2013)
LymphoblastHCC1937
vi)Withaferin AEpithelialMDA-MB-231, MCF-7ER stress, ROS production, Alix↓Ghosh et al. (2016)
vii)Deoxyelephantopin derivative (DETD)EpithelialMDA-MB-231Oxidative and ER stress, p-JNK↑Shiau et al. (2017)
viii)ChalcomoracinEpithelialMDA-MB-231ROS production, PINK1 ↑, Alix ↓, p-ERK↑Han et al. (2018)
ix)6-ShogaolEpithelialMDA-MB-231Proteasomal inhibition, ER stressNedungadi, et al. (2018)
x)PlumbaginEpithelialMDA-MB-231Disruption of sulfhydryl homeostasis and inhibition of proteasomeBinoy et al. (2019)
xi)2′-hydroxy-retrochalconeEpithelialMDA-MB-231Proteasomal dysfunction and ER stressNedungadi et al. (2021)
xii)Indirubin-3′-monoxime (I3M)EpithelialMDA-MB-231Proteasomal dysfunction and ER stress-mediated Ca2+ release.Dilshara et al. (2021)
xiii)Cannabinoids (C6 combination)EpithelialMDA-MB-231, MCF-7ER stress (GRP78 increase)Schoeman et al. (2020)
xiv)Gambogic AcidEpithelialMDA-MB-453, MDA-MB-468, MDA-MB-435SDisruption of thiol proteostasisSeo et al. (2019)
Melanocyte
xv)5,7-dibromo-8-(methoxymethoxy)-2-methylquinoline (HQ-11)EpithelialMDA-MB-231, MCF-7ER stress, proteasomal inhibition, pERK↑Ma et al. (2022)
xvi)GlabridinEpithelialMDA-MB-231, MCF-7ER stress, poly ubiquitinated protein accumulation, proteasome suppression, ROS production, MMP lossCui and Cui (2022)
xvii)Isoxazole derivative of usnic acidEpithelialMDA-MB-231, MCF-7ER stress, IP3R channel activationPyrczak-Felczykowska et al. (2022)
xviii)Derivative of pyrazolo[3,4-h]quinoline scaffold (YRL1091)EpithelialMDA-MB-231, MCF-7ER stress, accumulation of ubiquitinated proteins, ROS production, ERK↑, JNK↑, Alix↓Nguyen et al. (2022)
xix)Ginger extractEpithelialMDA-MB-231ER stress, mitochondrial dysfunction, AIF translocation and DNA damageNedungadi et al. (2021)
xx)Disulfiram oxy-derivativesEpithelialMCF-7ER stress, mitochondrial damage, 20S proteasome inhibition and actin depolymerization at later stagesSolovieva et al. (2022)
2. Brain
i)CurcuminGlioblastomaA172via microRNAs, AKT-Insulin, and p53-BCL2 networks, and AKT protein level reduction was confirmedGarrido-Armas et al. (2018)
ii)Ophiobolin APleomorphicastrocytoid, Neuronal, Fibroblast, Fibroblast) FibroblastU373-MG, U251N, U251MG, A172ER stress, NAC inhibition, decrease of BKCa channelBury et al. (2013)
T98G
iii)Oligomeric ProcyanidinsEpithelialU-87Extracellular Ca2+ influx, pERK1/2↑, p-p38 ↑(Zhang et al., 2010)
iv)PaclitaxelEpithelialU-87CHX has no effect, MEK, p38 and JNK pathways are not involvedSun et al. (2010)
v)YessotoxinMuscle cells from intracranial tumorBC3H1ER and mitochondrial swelling, p-JNK↑Korsnes et al. (2011)
vi)1-Desulfo YessotoxinMuscle cells from intracranial tumorBC3H1ER and mitochondrial swelling, p-p38↑Korsnes et al. (2013)
vii)XanthohumolEpithelialSH-SY5YER stress and LC3B upregulation, p38 ↑Mi et al. (2017)
3. Blood
i)HonokiolLymphoblastK562ROS generation ROS generation, ER stress, LC3 upregulation, mTOR and MAPK activatedLiu et al. (2021), Wang et al. (2013)
PromyelocyteNB4
ii)XanthohumolPromyeloblastHL-60ER stress and LC3B upregulation, p38 ↑Mi et al. (2017)
iii)Iturin lipopeptideLymphoblastK562LC3B and p62 upregulationZhao et al. (2019)
iv)BrassininLymphoblastK562ROS production, mitochondrial damage, ER stress, and activation of MAPKYang et al. (2023)
Lymphoblast-likeKBM5, LAMA84, and KCL22
4. Cervical
i)CelastrolEpithelialHeLaProteasome inhibition, Mitochondrial Ca2+ overload, pERK1/2↑, p-JNKs ↑, p-p38 ↑Wang et al. (2012)
ii)Cyclosporin AEpithelialHeLa, SiHaLC3 upregulation, Cyclophilin B↓, Alix↓Ram and Ramakrishna (2014)
iii)8-p-Hydroxybenzoyl tovarolEpithelialHeLaBip, CHOP, IRE1α and XBP1 upregulationZhang et al. (2015)
iv)Seleno-DL-CystineEpithelialHeLaBip and CHOP polyubiquitination upregulation, ROS generationWallenberg et al. (2014)
v)PaclitaxelEpithelialHeLaCHX has no effect, MEK, p38 and JNK are not involvedSun et al. (2010)
vi)Wheat germ AgglutininEpithelialHeLa, SiHa, CaSKiAutophagy-linked FYVE (Alfy) protein inhibition, ER stress, LC3B upregulationTsai et al. (2017)
vii)2′-hydroxy-retrochalconeEpithelialHeLaProteasomal dysfunction, ER stress, LC3 upregulationNedungadi et al. (2021)
5. Thyroid
i)TunicamycinEpithelial8505C, CAL62, FRO cell linesBip, CHOP, p-PERK and IRE1 upregulationKim et al. (2014)
6. Liver
i)HesperidinEpithelialHepG2Mitochondrial dysfunction and Ca2+ overload, p-ERK↑Yumnam et al., 2016)
ii)Cis-NerolidolEpithelialHepG2/C3 AER stress, increased activity of cytochrome P450 enzymesBiazi et al. (2017)
iii)Gambogic AcidEpithelial; diffusely spreading cellsSNU-449Proteasomal inhibition and ER stress, ROS independent- mitochondrial depolarizationSeo et al. (2019)
7. Colon
i)CurcuminEpithelialHCT116Proteasome inhibition ROS, Mitochondrial Ca2+ overload, LC3 upregulation, pERK1/2↑, p-JNKs↑, Alix↓Lee et al. (2015)
ii)CelastrolEpithelialDLD-1, RKOProteasome inhibition, Mitochondrial Ca2+ overload, pERK1/2↑, p-JNKs ↑, p-p38 ↑Yoon et al. (2014)
iii)15d-PGJ2EpithelialHCT116Disruption of sulfhydryl homeostasis LC3 upregulation, pERK1/2↑Kar et al. (2009)
iv)Ginsenoside Rh2EpithelialHCT116, SW480p53 activation, activation of death by antioxidantsLi et al. (2011), Wan et al. (2018)
v)ProtopanaxadiolEpithelialHCT116, SW480Death acceleration by inhibiting ROS generation, NF-κB activatedWang et al. (2013)
vi)ɣ-TocotrienolEpithelialSW620 and HCT-8Wnt signals↓ (β-catenin, cyclin D, c-Jun)Zhang et al. (2011) (2013)
δ-TocotrienolEpithelialSW620Wnt signals↓ (β-catenin, cyclin D, c-Jun)
vii)Iturin A-like lipopeptidesEpithelialCaco-2ER stress, ROS generation, Ca2+Zhao et al. (2019)
viii)LoperamideEpithelialDLD-1, SW-480, SW-620, HCT116ER stress, Ca2+ imbalance and CHOP↑Kim et al. (2019)
ix)Purified resin glycoside fraction (Pharbitidis Semen)EpithelialHT-29 and HCT-116Chloride intracellular channel-1 activation and intracellular Cl↑, MAPK activationZhu et al. (2019)
8. Prostate
i)CurcuminEpithelialPC-3MProteasome inhibition ROS, Mitochondrial Ca2+ overload, LC3 upregulation, pERK1/2↑, p-JNKs↑, Alix↓Lee et al. (2015)
ii)15d-PGJ2EpithelialDU145Disruption of sulfhydryl homeostasis LC3 upregulation, pERK1/2↑Kar et al. (2009)
iii)Benzo[a]quinolizidine analogsEpithelialPC3ER stress and LC3B upregulationZheng et al. 2016)
iv)ChalcomoracinEpithelialLNCaP, PC-3ROS generation, ER stress, PINK1 ↑, Alix ↓, p-ERK↑Han et al, 2018)
v)δ-TocotrienolEpithelialCRPC cells—DU145, PC-3ER stress, LC3 and p62 upregulation, p-JNK ↑, p-p38 ↑Fontana et al. (2020)
9. Ovarian
i)MorusinEpithelialA2780, HO-8910, SKOV3Ca2+ overload, ROS generation and loss of mitochondrial membrane potentialXue et al. (2018)
ii)ElaiophylinEpithelialSKOV3, OVCAR8, UWB1.289, SW626ER stress, SHP2/SOS1/MAPK↑Li et al. (2022)
10. Lung
(i)Cyclosporin AEpithelialA549LC3 upregulation, Cyclophilin B↓, Alix↓Ram and Ramakrishna (2014)
ii)PaclitaxelEpithelialA549CHX has no effect, MEK, p38 and JNK are not involvedGuo et al. (2010)
EpithelialASTC-a-1
iii)6-ShogaolEpithelialA549Proteasome inhibition, ER stress, ROS generation, LC3 upregulationNedungadi et al. (2018)
iv)Hinokitiol copper complexEpithelialA549Proteasome inhibition, ER stressChen et al. (2017)
v)ChalcomoracinEpithelialH460ER stress, MAPK activationHan et al. (2018)
EpithelialA549
AdenocytePC-9
vi)Paris Saponin II (PSII)EpithelialNCI-H460ER stress, JNK pathway activationMan et al. (2020)
EpithelialNCI-H520
vii)Prenylated bibenzyls (Radula constricta)EpithelialA549, NCI-H1299ROS elevation and loss in mitochondrial membrane potentialZhang et al. (2019)
viii)Gambogic AcidEpithelialNCI-H460Proteasomal inhibition and ER stress, ROS independent- mitochondrial depolarizationSeo et al. (2019)
ix)Epimedokoreanin BEpithelialA549, NCL-H292ER stress, autophagosome accumulation, ROS production, loss of MMP, UPR signalingZheng et al. (2022)
x)DHW-221EpithelialA549ER stress, PI3K/mTOR inhibition, MAPK activationLiu et al. (2022)
xi)Ginger extractEpithelialA549ER stress, mitochondrial dysfunction, AIF translocation and DNA damageNedungadi et al. (2021)
11. Skin
i)Cyclosporin AKeratinocyteHaCaTLC3 upregulation, Cyclophilin B↓, Alix↓(Ram and Ramakrishna (2014)
ii)δ-tocotrienolEpithelialA375Ca2+ overload and ROS generation, MAPK activationRaimondi et al. (2021)
12. Bone
i)Cyclosporin AEpithelialU2OS, Saos-2LC3 upregulation, Cyclophilin B↓, Alix↓Ram and Ramakrishna (2014)
13. Kidney and Bladder
i)Jolkinolide BEpithelialT24, UM-UC-3, T24/CDDPROS-mediated ER stress, MAPK and ERK activationSang et al. (2021)
14. Oral
i)Isorhamnetin (3′-Methoxy-3,4′,5,7-tetrahydroxyflavone)EpithelialHSC-3, HSC-4, PE/CA-PJ15↑ROS generation, ERK/MAPKChen et al. (2021)
15. Pancreas
i)Gambogic AcidEpithelialBxPC-3Proteasomal inhibition and ER stress, ROS- independent mitochondrial depolarizationSeo et al. (2019)
16. Stomach
i)Gambogic AcidEpithelialSNU-668 (gastric cancer)Proteasomal inhibition and ER stress, ROS independent- mitochondrial depolarizationSeo et al. 2019)

Paraptosis-inducing compounds against cancer cell lines.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

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Publisher’s note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Summary

Keywords

cancer, paraptosis, programmed cell death, alternative cell death, cancer therapy, apoptosis

Citation

Hanson S, Dharan A, V. JP, Pal S, Nair BG, Kar R and Mishra N (2023) Corrigendum: Paraptosis: a unique cell death mode for targeting cancer. Front. Pharmacol. 14:1274076. doi: 10.3389/fphar.2023.1274076

Received

07 August 2023

Accepted

25 August 2023

Published

08 September 2023

Volume

14 - 2023

Edited and reviewed by

Zhaoshi Bai, The Affiliated Cancer Hospital of Nanjing Medical University, China

Updates

Copyright

*Correspondence: Nandita Mishra,

†These authors have contributed equally to this work and share first authorship

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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