ArticleOncogene1999
Inhibition of Bcl-xL expression sensitizes normal human keratinocytes and epithelial cells to apoptotic stimuli.
Article in Oncogene, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 89 citations in OpenAlex.
- Endogenous and imposed determinants of apoptotic vulnerabilities in cancer.Trends in cancer · 2023Review
- Antioxidant Activities and Protective Effects of Dendropachol, a New Bisbibenzyl Compound fromAntioxidants (Basel, Switzerland) · 2021Article
- The small molecule Retro-1 enhances the pharmacological actions of antisense and splice switching oligonucleotides.Nucleic acids research · 2013Article
- Functional characterization of CLPTM1L as a lung cancer risk candidate gene in the 5p15.33 locus.PloS one · 2012Article
- Targeted disruption of Bcl-xL in mouse keratinocytes inhibits both UVB- and chemically induced skin carcinogenesis.Molecular carcinogenesis · 2009Article
- Expression of Bcl-2 family proteins in psoriasis.Croatian medical journal · 2007Article
- Distinct promoters mediate constitutive and inducible Bcl-XL expression in malignant lymphocytes.Oncogene · 2007Article
- Curcumin induces G2/M arrest and apoptosis in cisplatin-resistant human ovarian cancer cells by modulating Akt and p38 MAPK.Cancer biology & therapy · 2007Article
- Serpin squamous cell carcinoma antigen inhibits UV-induced apoptosis via suppression of c-JUN NH2-terminal kinase.The Journal of cell biology · 2006Article
- Modulation of 5' splice site selection using tailed oligonucleotides carrying splicing signals.BMC biotechnology · 2006Article
- Resistance to chemotherapy-induced apoptosis via decreased caspase-3 activity and overexpression of antiapoptotic proteins in ovarian cancer.Journal of cancer research and clinical oncology · 2004Article
- Antisense oligonucleotide-based therapeutics for cancer.Oncogene · 2003Review
- Bcl-x(L) antisense oligonucleotides radiosensitise colon cancer cells.British journal of cancer · 2003Article
- Gene expressions in Jurkat cells poisoned by a sulphur mustard vesicant and the induction of apoptosis.British journal of pharmacology · 2002Article
- The expression of antiapoptotic proteins Bcl-2, Bcl-X(L), and Mcl-1 in benign, dysplastic, and malignant biliary epithelium.Journal of clinical pathology · 2001Article
- Constitutively activated Stat3 protects fibroblasts from serum withdrawal and UV-induced apoptosis and antagonizes the proapoptotic effects of activated Stat1.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Bcl-X(L) antisense sensitizes human colon cancer cell line to 5-fluorouracil.Japanese journal of cancer research : Gann · 2000Article
- Activated Ras prevents downregulation of Bcl-X(L) triggered by detachment from the extracellular matrix. A mechanism of Ras-induced resistance to anoikis in intestinal epithelial cells.The Journal of cell biology · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epidermis is continually exposed to harmful mutagens that have the potential to cause DNA damage. To protect the skin from accumulating mutated cells, keratinocytes have developed a highly regulated mechanism of eliminating damaged cells through apoptosis. Bcl-xL is a well-described cell survival protein that when overexpressed in skin can protect keratinocytes from UV radiation-induced apoptosis. To begin to unravel the complex mechanisms that keratinocytes use to survive, we wanted to characterize the role of endogenous Bcl-xL in protecting cells from death. In this study, we describe the development and characterization of an antisense inhibitor to Bcl-xL. We show that this inhibitor reduces Bcl-xL RNA and protein in a concentration-dependent, sequence-specific manner. Furthermore, treatment of keratinocytes and epithelial cells with this inhibitor sensitizes these cells to UV-B radiation and cisplatinum treatment-induced apoptosis. Thus, these results offer direct evidence that Bcl-xL is critical in the protection of skin and epithelial cells from apoptosis and provide a basis for the role of Bcl-xL in keratinocyte and epithelial cell survival.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.