ArticleInternational journal of clinical and experimental medicine2015
Effect of Smac in combination with cisplatin on esophageal cancer cell line ECA109.
Article in International journal of clinical and experimental medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Research progress of ginseng active ingredients combined with chemotherapy in cancer therapy.Journal of ginseng research · 2026Review
- SMAC exhibits anti-tumor effects in ECA109 cells by regulating expression of inhibitor of apoptosis protein family.World journal of clinical cases · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThis study was to investigate inhibiting effect of structurally unique Second mitochondria-derived activator of caspase (Smac) in combination with cisplatin on esophageal cancer cell line ECA109.
methodsPcDNA3.1-Smac (ECA109/Smac group), pcDNA3.1 (ECA109/neo group) and PBS (ECA109 or control group) were transfected into ECA109 cells respectively, and transfected cells which expressed Smac stably were got. Smac protein expression was analyzed by Western blot. The invasive ability of cells was examined. Flow cytometry was used to analyze apoptosis induced by cisplatin with Annexin V/PI double staining technique.
resultsSmac gene was successfully transfected into ECA109 cell, over-expression of Smac could decrease cell invasive ability obviously compared to control group (P<0.05). Apoptosis rate of cells induced by cisplatin in ECA109/Smac group was significant higher than that in ECA109/neo and ECA109 group (P<0.05).
conclusionIt indicated that over-expression of Smac increases the sensitivity of esophageal cancer ECA109 cells to cisplatin treatment, combination of conventional anticancer drug with Smac may be beneficial for the treatment of esophageal cancer.
Indexed as
Identifiers
26770460PMC4694360W2335881009What 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.