The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.
Mechanism of chemoresistance mediated by miR-140 in human osteosarcoma and colon cancer cells
Open accessAbstract
In this study, high-throughput microRNA (miRNA) expression analysis revealed that the expression of miR-140 was associated with chemosensitivity in osteosarcoma tumor xenografts. Tumor cells ectopically transfected with miR-140 were more resistant to methotrexate and 5-fluorouracil (5-FU). Overexpression of miR-140 inhibited cell proliferation in both osteosarcoma U-2 OS (wt-p53) and colon cancer HCT 116 (wt-p53) cell lines, but less so in osteosarcoma MG63 (mut-p53) and colon cancer HCT 116 (null-p53) cell lines. miR-140 induced p53 and p21 expression accompanied with G1 and G2 phase arrest only in cell lines containing wild type of p53. Histone deacetylase 4 (HDAC4) was confirmed to be one of the important targets of miR-140. The expression of endogenous miR-140 was significantly elevated in CD133+hiCD44+hi colon cancer stem-like cells that exhibit slow proliferating rate and chemoresistance. Blocking endogenous miR-140 by locked nucleic acid-modified anti-miR partially sensitized resistant colon cancer stem-like cells to 5-FU treatment. Taken together, our findings indicate that miR-140 is involved in the chemoresistance by reduced cell proliferation through G1 and G2 phase arrest mediated in part through the suppression of HDAC4. miR-140 may be a candidate target to develop novel therapeutic strategy to overcome drug resistance.
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Bartel (2004) · doi:10.1016/s0092-8674(04)00045-5 · Cited by 34,714
A microRNA component of the p53 tumour suppressor network
He, L., He, X., Lim, L. P., de Stanchina, E., Xuan, Z., Liang, Y., Xue, W., Zender, L., Magnus, J., Ridzon, D., et al. (2007) · Nature · doi:10.1038/nature05939 · Cited by 2,692
Disruption of p53 in human cancer cells alters the responses to therapeutic agents.
Bunz, F., Hwang, P. M., Torrance, C., Waldman, T., Zhang, Y., Dillehay, L., Williams, J., Lengauer, C., Kinzler, K. W., & Vogelstein, B. (1999) · Journal of Clinical Investigation · doi:10.1172/jci6863 · Cited by 1,044
The cartilage specific microRNA‐140 targets histone deacetylase 4 in mouse cells
Tuddenham, L., Wheeler, G., Ntounia-Fousara, S., Waters, J., Hajihosseini, M. K., Clark, I., & Dalmay, T. (2006) · FEBS Letters · doi:10.1016/j.febslet.2006.06.080 · Cited by 422
Cited by
Epigenetic Alterations in Colorectal Cancer: Emerging Biomarkers
Okugawa, Y., Grady, W. M., & Goel, A. (2015) · Gastroenterology · doi:10.1053/j.gastro.2015.07.011 · Cited by 782
Interplay between microRNAs and the epigenetic machinery: An intricate network
Iorio, M. V., Piovan, C., & Croce, C. M. (2010) · Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms · doi:10.1016/j.bbagrm.2010.05.005 · Cited by 306
Lilienthal, I., & Herold, N. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21186885 · Cited by 283
Bitarte, N., Bandres, E., Boni, V., Zarate, R., Rodriguez, J., Gonzalez-Huarriz, M., Lopez, I., Javier Sola, J., Alonso, M. M., Fortes, P., et al. (2011) · Stem Cells · doi:10.1002/stem.741 · Cited by 272
The role of microRNAs in colorectal cancer
Schetter, A. J., Okayama, H., & Harris, C. C. (2012) · The Cancer Journal · doi:10.1097/ppo.0b013e318258b78f · Cited by 252
Metadata
- Authors
- Song, B., Wang, Y., Xi, Y., Kudo, K., Bruheim, S., Botchkina, G. I., Gavin, E., Wan, Y., Formentini, A., Kornmann, M., Fodstad, O., & Ju, J.
- Venue
- Oncogene
- Published
- 2009-09-07
- Volume
- 28
- Issue
- 46
- Pages
- 4065-4074
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2088230889
- Cited by
- 410
- References
- 4
- FWCI
- 7.77
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Song, B., Wang, Y., Xi, Y., Kudo, K., Bruheim, S., Botchkina, G. I., Gavin, E., Wan, Y., Formentini, A., Kornmann, M., Fodstad, O., & Ju, J. (2009). Mechanism of chemoresistance mediated by miR-140 in human osteosarcoma and colon cancer cells. Oncogene. https://doi.org/10.1038/onc.2009.274
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