The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Mcl-1 promotes lung cancer cell migration by directly interacting with VDAC to increase mitochondrial Ca2+ uptake and reactive oxygen species generation
Open accessAbstract
Mcl-1 is an antiapoptotic member of the Bcl-2 family frequently upregulated in non-small cell lung carcinoma (NSCLC). We now report the physiological significance of an interaction between Mcl-1 and the mitochondrial outer membrane-localized voltage-dependent anion channel (VDAC) in NSCLC cell lines. Mcl-1 bound with high affinity to VDAC1 and 3 isoforms but only very weakly to VDAC2 and binding was disrupted by peptides based on the VDAC1 sequence. In A549 cells, reducing Mcl-1 expression levels or application of VDAC-based peptides limited Ca 2+ uptake into the mitochondrial matrix, the consequence of which was to inhibit reactive oxygen species (ROS) generation. In A549, H1299 and H460 cells, both Mcl-1 knockdown and VDAC-based peptides attenuated cell migration without affecting cell proliferation. Migration was rescued in Mcl-1 knockdown cells by experimentally restoring ROS levels, consistent with a model in which ROS production drives increased migration. These data suggest that an interaction between Mcl-1 and VDAC promotes lung cancer cell migration by a mechanism that involves Ca 2+-dependent ROS production.
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Cited by
Cloonan, S. M., & Choi, A. M. K. (2016) · Journal of Clinical Investigation · doi:10.1172/jci81113 · Cited by 322
La Rovere, R. M. L., Roest, G., Bultynck, G., & Parys, J. B. (2016) · Cell Calcium · doi:10.1016/j.ceca.2016.04.005 · Cited by 257
VDAC1 at the crossroads of cell metabolism, apoptosis and cell stress
Shoshan-Barmatz, V., N. Maldonado, E., & Krelin, Y. (2017) · Cell Stress · doi:10.15698/cst2017.10.104 · Cited by 170
Metadata
- Authors
- Huang, H., Shah, K., Bradbury, N. A., Li, C., & White, C.
- Venue
- Cell Death & Disease
- Published
- 2014-10-23
- Volume
- 5
- Issue
- 10
- Pages
- e1482-e1482
- ISSN
- 2041-4889 (ISSN-L)
- OpenAlex
- W2065915608
- Cited by
- 163
- References
- 15
- FWCI
- 6.45
- Type
- journal article
- Language
- en
- Open access
- gold
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- Huang, H., Shah, K., Bradbury, N. A., Li, C., & White, C. (2014). Mcl-1 promotes lung cancer cell migration by directly interacting with VDAC to increase mitochondrial Ca2+ uptake and reactive oxygen species generation. Cell Death & Disease. https://doi.org/10.1038/cddis.2014.419
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