RETRACTED: Identification of Nrf2/STAT3 axis in induction of apoptosis through sub‐G<sub>1</sub> cell cycle arrest mechanism in HT‐29 colon cancer cells
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Post-publication record
- Nature
- Retraction
- Reason
- Concerns/Issues about Data;Euphemisms for Plagiarism;Investigation by Journal/Publisher;Investigation by Third Party;Objections by Author(s);Plagiarism of Image;Unreliable Data;Unreliable Results and/or Conclusions;
- Date
- 9/12/2024 0:00
- Flagged by OpenAlex?
- Yes
Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.
Abstract
We investigated the role of stattic as an adjuvant molecule to increase the cytotoxicity of 5-fluorouracil (5-FU) through specific inhibition of molecular targets, signal transducer and activator of transcription 3 (STAT3) and nuclear factor erythroid 2-related factor 2 (Nrf2) in HT-29 colon cancer cells. Cytotoxicity and apoptotic effects were investigated by methylthiazolyldiphenyl-tetrazolium bromide assay and flow cytometry analysis, respectively. Real-time polymerase chain reaction was applied to assess the messenger RNA (mRNA) level of STAT3, Nrf2, and apoptotic genes including Bax, Bcl-xl, and Bcl-2. The antitumor effect of 5-FU in combination with stattic induced synergistic effect in HT-29 cells with combination indexes (CIs) 0.49. Flow cytometric results related to apoptotic confirmed that there was up to 40% increase in the population of apoptotic cells in HT-29 colon cancer cells incubated with 5-FU and stattic compared with control groups. Our data from gene expression determined a substantial diminish in the mRNA levels of the Nrf2 and antiapoptotic gene Bcl-2 along with a noticeable increase in the level of the proapoptotic Bax in HT-29 colon cells that underwent cotreatment with 5-FU and stattic (P < 0.05). Moreover, the results exhibited that stattic can be used as adjuvant chemotherapy besides the 5-FU. This therapeutic approach in colon cancer could mediate 5-FU chemoresistance via modulating therapeutic targets (ie, STAT3 and Nrf2 pathways) and decreased 5-FU-related adverse effects.
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The record
- Venue
- Journal of Cellular Biochemistry
- Topic
- Cytokine Signaling Pathways and Interactions
- Field
- Medicine
- Canadian institutions
- University of Alberta
- Funders
- Drug Applied Research Center, Tabriz University of Medical SciencesUniversity of Tabriz
- Keywords
- ApoptosisMechanism (biology)Identification (biology)Cell biologyChemistryCell cycle checkpointSTAT3Cancer researchCell cycleBiologyBiochemistryPhysics
- Has abstract in OpenAlex
- yes