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Article ; Online: T-type channels in cancer cells: Driving in reverse.

Alza, Lía / Visa, Anna / Herreros, Judit / Cantí, Carles

2022 Volume 105, Page(s) 102610

Abstract: In the strongly polarized membranes of excitable cells, activation of T-type ... ...

Abstract	In the strongly polarized membranes of excitable cells, activation of T-type Ca
MeSH term(s)	Action Potentials/physiology ; Calcium/metabolism ; Neoplasms
Chemical Substances	Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-06-06
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	757687-0
ISSN	1532-1991 ; 0143-4160
ISSN (online)	1532-1991
ISSN	0143-4160
DOI	10.1016/j.ceca.2022.102610
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Zs.A 1596: Show issues

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Article ; Online: Tetralol derivative NNC-55-0396 induces glioblastoma cell death by activating IRE1α, JNK1 and calcium signaling.

Visa, Anna / Alza, Lía / Cantí, Carles / Herreros, Judit

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2022 Volume 149, Page(s) 112881

Abstract: Mibefradil and NNC-55-0396, tetralol derivatives with a proven -ability to block T-type calcium channels in excitable cells, reduce cancer cell viability in vitro, causing cell death. Furthermore, they reduce tumor growth in preclinical models of ... ...

Abstract	Mibefradil and NNC-55-0396, tetralol derivatives with a proven -ability to block T-type calcium channels in excitable cells, reduce cancer cell viability in vitro, causing cell death. Furthermore, they reduce tumor growth in preclinical models of Glioblastoma multiforme (GBM), a brain tumor of poor prognosis. Here we found that GBM cells treated with cytotoxic concentrations of NNC-55-0396 paradoxically increased cytosolic calcium levels through the activation of inositol triphosphate receptors (IP
MeSH term(s)	Apoptosis ; Benzimidazoles ; Calcium/metabolism ; Calcium Signaling ; Cell Death ; Cyclopropanes ; Endoplasmic Reticulum Stress/genetics ; Endoribonucleases/genetics ; Endoribonucleases/metabolism ; Glioblastoma/drug therapy ; Glioblastoma/pathology ; Humans ; Naphthalenes ; Protein Serine-Threonine Kinases/genetics ; Tetralones ; Unfolded Protein Response
Chemical Substances	Benzimidazoles ; Cyclopropanes ; Naphthalenes ; Tetralones ; NNC 55-0396 (0A7CE46ERM) ; tetralol (530-91-6) ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; Endoribonucleases (EC 3.1.-) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-03-31
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2022.112881
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Article ; Online: Tetralol derivative NNC-55-0396 targets hypoxic cells in the glioblastoma microenvironment: an organ-on-chip approach.

Bayona, Clara / Alza, Lía / Ranđelović, Teodora / Sallán, Marta C / Visa, Anna / Cantí, Carles / Ochoa, Ignacio / Oliván, Sara / Herreros, Judit

Cell death & disease

2024 Volume 15, Issue 2, Page(s) 127

Abstract: Glioblastoma (GBM) is a highly malignant brain tumour characterised by limited treatment options and poor prognosis. The tumour microenvironment, particularly the central hypoxic region of the tumour, is known to play a pivotal role in GBM progression. ... ...

Abstract	Glioblastoma (GBM) is a highly malignant brain tumour characterised by limited treatment options and poor prognosis. The tumour microenvironment, particularly the central hypoxic region of the tumour, is known to play a pivotal role in GBM progression. Cells within this region adapt to hypoxia by stabilising transcription factor HIF1-α, which promotes cell proliferation, dedifferentiation and chemoresistance. In this study we sought to examine the effects of NNC-55-0396, a tetralol compound which overactivates the unfolded protein response inducing apoptosis, using the organ-on-chip technology. We identified an increased sensitivity of the hypoxic core of the chip to NNC, which correlates with decreasing levels of HIF1-α in vitro. Moreover, NNC blocks the macroautophagic process that is unleashed by hypoxia as revealed by increased levels of autophagosomal constituent LC3-II and autophagy chaperone p62/SQSTM1. The specific effects of NNC in the hypoxic microenvironment unveil additional anti-cancer abilities of this compound and further support investigations on its use in combined therapies against GBM.
MeSH term(s)	Humans ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Hypoxia/metabolism ; Cell Line, Tumor ; Brain Neoplasms/drug therapy ; Brain Neoplasms/genetics ; Brain Neoplasms/metabolism ; Tumor Microenvironment ; Benzimidazoles ; Cyclopropanes ; Naphthalenes ; Tetralones
Chemical Substances	NNC 55-0396 (0A7CE46ERM) ; tetralol (530-91-6) ; Benzimidazoles ; Cyclopropanes ; Naphthalenes ; Tetralones
Language	English
Publishing date	2024-02-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-024-06492-1
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Article ; Online: The rise of T-type channels in melanoma progression and chemotherapeutic resistance.

Alza, Lía / Visa, Anna / Herreros, Judit / Cantí, Carles

Biochimica et biophysica acta. Reviews on cancer

2020 Volume 1873, Issue 2, Page(s) 188364

Abstract: Hyperactivation of the Mitogen Activated Protein Kinase (MAPK) pathway is prevalent in melanoma, principally due to mutations in the BRAF and NRAS genes. MAPK inhibitors are effective only short-term, and recurrence occurs due to functional redundancies ... ...

Abstract	Hyperactivation of the Mitogen Activated Protein Kinase (MAPK) pathway is prevalent in melanoma, principally due to mutations in the BRAF and NRAS genes. MAPK inhibitors are effective only short-term, and recurrence occurs due to functional redundancies or intertwined pathways. The remodeling of Ca
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Calcium Channel Blockers/pharmacology ; Calcium Channel Blockers/therapeutic use ; Calcium Channels, T-Type/metabolism ; Cell Line, Tumor ; Disease Progression ; Drug Resistance, Neoplasm/drug effects ; Drug Resistance, Neoplasm/genetics ; GTP Phosphohydrolases/antagonists & inhibitors ; GTP Phosphohydrolases/genetics ; Humans ; Kaplan-Meier Estimate ; MAP Kinase Signaling System/drug effects ; MAP Kinase Signaling System/genetics ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/mortality ; Melanoma/pathology ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/genetics ; Mutation ; Prognosis ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Proto-Oncogene Proteins B-raf/antagonists & inhibitors ; Proto-Oncogene Proteins B-raf/genetics ; Skin Neoplasms/drug therapy ; Skin Neoplasms/genetics ; Skin Neoplasms/mortality ; Skin Neoplasms/pathology ; Treatment Outcome
Chemical Substances	Antineoplastic Agents ; Calcium Channel Blockers ; Calcium Channels, T-Type ; Membrane Proteins ; Protein Kinase Inhibitors ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; GTP Phosphohydrolases (EC 3.6.1.-) ; NRAS protein, human (EC 3.6.1.-)
Language	English
Publishing date	2020-04-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2918802-7
ISSN	1879-2561 ; 0304-419X
ISSN (online)	1879-2561
ISSN	0304-419X
DOI	10.1016/j.bbcan.2020.188364
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Zs.A 7162: Show issues

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Article: FAK Inhibition Induces Glioblastoma Cell Senescence-Like State through p62 and p27.

Alza, Lía / Nàger, Mireia / Visa, Anna / Cantí, Carles / Herreros, Judit

Cancers

2020 Volume 12, Issue 5

Abstract: Focal adhesion kinase (FAK) is a central component of focal adhesions that regulate cancer cell proliferation and migration. Here, we studied the effects of FAK inhibition in glioblastoma (GBM), a fast growing brain tumor that has a poor prognosis. ... ...

Abstract	Focal adhesion kinase (FAK) is a central component of focal adhesions that regulate cancer cell proliferation and migration. Here, we studied the effects of FAK inhibition in glioblastoma (GBM), a fast growing brain tumor that has a poor prognosis. Treating GBM cells with the FAK inhibitor PF-573228 induced a proliferative arrest and increased cell size. PF-573228 also reduced the growth of GBM neurospheres. These effects were associated with increased p27/CDKN1B levels and β-galactosidase activity, compatible with acquisition of senescence. Interestingly, FAK inhibition repressed the expression of the autophagy cargo receptor p62/SQSTM-1. Moreover, depleting p62 in GBM cells also induced a senescent-like phenotype through transcriptional upregulation of
Language	English
Publishing date	2020-04-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers12051086
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Article ; Online: Targeting T-type channels in cancer: What is on and what is off?

Visa, Anna / Alza, Lía / Casas-Benito, Adrian / Herreros, Judit / Cantí, Carles

Drug discovery today

2021 Volume 27, Issue 3, Page(s) 743–758

Abstract: Over the past 20 years, various studies have demonstrated a pivotal role of T-type calcium channels (TTCCs) in tumor progression. Cytotoxic effects of TTCC pharmacological blockers have been reported in vitro and in preclinical models. However, their ... ...

Abstract	Over the past 20 years, various studies have demonstrated a pivotal role of T-type calcium channels (TTCCs) in tumor progression. Cytotoxic effects of TTCC pharmacological blockers have been reported in vitro and in preclinical models. However, their roles in cancer physiology are only beginning to be understood. In this review, we discuss evidence for the signaling pathways and cellular processes stemming from TTCC activity, mainly inferred by inverse reasoning from pharmacological blocks and, only in a few studies, by gene silencing or channel activation. A thorough analysis indicates that drug-induced cytotoxicity is partially an off-target effect. Dissection of on/off-target activity is paramount to elucidate the physiological roles of TTCCs, and to deliver efficacious therapies suited to different cancer types and stages.
MeSH term(s)	Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Calcium Channel Blockers/pharmacology ; Calcium Channels, T-Type/genetics ; Calcium Channels, T-Type/metabolism ; Humans ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Signal Transduction
Chemical Substances	Antineoplastic Agents ; Calcium Channel Blockers ; Calcium Channels, T-Type
Language	English
Publishing date	2021-11-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1324988-5
ISSN	1878-5832 ; 1359-6446
ISSN (online)	1878-5832
ISSN	1359-6446
DOI	10.1016/j.drudis.2021.11.021
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Zs.A 4725: Show issues

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Article ; Online: The Hard-To-Close Window of T-Type Calcium Channels.

Visa, Anna / Shaikh, Soni / Alza, Lía / Herreros, Judit / Cantí, Carles

Trends in molecular medicine

2019 Volume 25, Issue 7, Page(s) 571–584

Abstract: T-Type calcium channels (TTCCs) are key regulators of membrane excitability, which is the reason why TTCC pharmacology is subject to intensive research in the neurological and cardiovascular fields. TTCCs also play a role in cancer physiology, and ... ...

Abstract	T-Type calcium channels (TTCCs) are key regulators of membrane excitability, which is the reason why TTCC pharmacology is subject to intensive research in the neurological and cardiovascular fields. TTCCs also play a role in cancer physiology, and pharmacological blockers such as tetralols and dihydroquinazolines (DHQs) reduce the viability of cancer cells in vitro and slow tumor growth in murine xenografts. However, the available compounds are better suited to blocking TTCCs in excitable membranes rather than TTCCs contributing window currents at steady potentials. Consistently, tetralols and dihydroquinazolines exhibit cytostatic/cytotoxic activities at higher concentrations than those required for TTCC blockade, which may involve off-target effects. Gene silencing experiments highlight the targetability of TTCCs, but further pharmacological research is required for TTCC blockade to become a chemotherapeutic option.
MeSH term(s)	Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channel Blockers/therapeutic use ; Calcium Channels, T-Type/chemistry ; Calcium Channels, T-Type/genetics ; Calcium Channels, T-Type/metabolism ; Cell Survival/drug effects ; Disease Susceptibility ; Gene Knockdown Techniques ; Humans ; Ion Channel Gating ; Signal Transduction
Chemical Substances	Calcium Channel Blockers ; Calcium Channels, T-Type
Language	English
Publishing date	2019-04-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036490-8
ISSN	1471-499X ; 1471-4914
ISSN (online)	1471-499X
ISSN	1471-4914
DOI	10.1016/j.molmed.2019.03.001
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Zs.A 4345: Show issues

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Article ; Online: Bafilomycin-A1 and ML9 Exert Different Lysosomal Actions to Induce Cell Death.

Shaikh, Soni / Nandy, Suman K / Cantí, Carles / Lavandero, Sergio

Current molecular pharmacology

2019 Volume 12, Issue 4, Page(s) 261–271

Abstract: Objective: Bafilomycin-A1 and ML9 are lysosomotropic agents, irrespective of cell types. However, the mechanisms of lysosome targeting either bafilomycin-A1 or ML9 are unclear.: Methods: The present research has been carried out by different ... ...

Abstract	Objective: Bafilomycin-A1 and ML9 are lysosomotropic agents, irrespective of cell types. However, the mechanisms of lysosome targeting either bafilomycin-A1 or ML9 are unclear. Methods: The present research has been carried out by different molecular and biochemical analyses like western blot, confocal imaging and FACS studies, as well as molecular docking. Results: Our data shows that pre-incubation of neonatal cardiomyocytes with ML9 for 4h induced cell death, whereas a longer period of time (24h) with bafilomycin-A1 was required to induce an equivalent effect. Neither changes in ROS nor ATP production is associated with such death mechanisms. Flow cytometry, LC3-II expression levels, and LC3-GFP puncta formation revealed a similar lysosomotropic effect for both compounds. We used a molecular docking approach, that predicts a stronger inhibitory activity against V-ATPase-C1 and C2 domains for bafilomycin-A1 in comparison to ML9. Conclusion: Bafilomycin-A1 and ML9 are lysosomotropic agents, involved in cell death events. But such death events are not associated with ATP and ROS production. Furthermore, both the drugs target lysosomes through different mechanisms. For the latter, cell death is likely due to lysosomal membrane permeabilization and release of lysosomal proteases into the cytosol.
MeSH term(s)	Animals ; Cell Death/drug effects ; Cells, Cultured ; Lysosomes/drug effects ; Lysosomes/metabolism ; Macroautophagy/drug effects ; Macrolides/pharmacology ; Models, Molecular ; Myocytes, Cardiac/cytology ; Myocytes, Cardiac/drug effects ; Piperazines/pharmacology ; Rats, Sprague-Dawley ; Reactive Oxygen Species/metabolism ; Sodium-Potassium-Exchanging ATPase/metabolism
Chemical Substances	Macrolides ; Piperazines ; Reactive Oxygen Species ; bafilomycin A1 (88899-55-2) ; Sodium-Potassium-Exchanging ATPase (EC 7.2.2.13)
Language	English
Publishing date	2019-03-01
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1874-4702
ISSN (online)	1874-4702
DOI	10.2174/1874467212666190308131250
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Article ; Online: T-type Ca

Sallán, Marta C / Visa, Anna / Shaikh, Soni / Nàger, Mireia / Herreros, Judit / Cantí, Carles

Cancer research

2018 Volume 78, Issue 3, Page(s) 603–609

Abstract: In the past decade, T-type ... ...

Abstract	In the past decade, T-type Ca
MeSH term(s)	Antineoplastic Agents/pharmacology ; Calcium Channel Blockers/pharmacology ; Calcium Channels, T-Type/chemistry ; Humans ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology
Chemical Substances	Antineoplastic Agents ; Calcium Channel Blockers ; Calcium Channels, T-Type
Language	English
Publishing date	2018-01-17
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-17-3061
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Article ; Online: T-Type Ca

Visa, Anna / Sallán, Marta C / Maiques, Oscar / Alza, Lía / Talavera, Elisabet / López-Ortega, Ricard / Santacana, Maria / Herreros, Judit / Cantí, Carles

Cancer research

2019 Volume 79, Issue 8, Page(s) 1857–1868

Abstract: ... T-type ... ...

Abstract	T-type Ca
MeSH term(s)	Animals ; Antineoplastic Agents, Alkylating/pharmacology ; Apoptosis ; Brain Neoplasms/drug therapy ; Brain Neoplasms/metabolism ; Brain Neoplasms/pathology ; Calcium Channels, T-Type/genetics ; Calcium Channels, T-Type/metabolism ; Cell Proliferation ; Disease Progression ; Gene Expression Regulation, Neoplastic/drug effects ; Glioblastoma/drug therapy ; Glioblastoma/metabolism ; Glioblastoma/pathology ; Humans ; Male ; Mice ; Mice, SCID ; Temozolomide/pharmacology ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Antineoplastic Agents, Alkylating ; CACNA1G protein, human ; Calcium Channels, T-Type ; Temozolomide (YF1K15M17Y)
Language	English
Publishing date	2019-02-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1432-1
ISSN	1538-7445 ; 0008-5472
ISSN (online)	1538-7445
ISSN	0008-5472
DOI	10.1158/0008-5472.CAN-18-1924
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