ArticleDiscover oncology2024
Anti-tumor activity of butorphanol in colorectal cancer via targeting SIGMAR1.
Article in Discover oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Suppression of SIGMAR1 hinders oral cancer cell growth via modulation of mitochondrial CaMolecular biology reports · 2025Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) stands for a prevailing gastrointestinal neoplasm, concomitant with considerable occurrence and lethality rate. Butorphanol, a synthetic opioid analgesic medication targeting the opiate receptor, has been recently reckoned to harbor anti-oncogenic properties. This study proposes to delineate the impacts of butorphanol on CRC and the interrelated response mechanism. In sigma non-opioid intracellular receptor 1 (SIGMAR1)-overexpressing CRC cells treated by varying concentrations of butorphanol, the functional experiments including CCK-8 method, EDU staining, wound healing and transwell assays severally appraised the capabilities for CRC cells to proliferate, migrate as well as invade. TUNEL staining assayed the cellular apoptotic level. The expressions of proteins implicated in proliferation, metastasis as well as apoptosis were ascertained by Western blot. CB-Dock2 server predicated butorphanol-SIGMAR1 interaction and Western blot also examined SIGMAR1 expression. Noticeably, butorphanol profoundly eliminated the capabilities of CRC cells to proliferate, migrate and invade whilst intensified the cellular apoptotic level with the ascending doses. Butorphanol was identified to possess an interrelation with SIGMAR1 and concentration-dependently lowered SIGMAR1 expression. Elevation of SIGMAR1 partially blunted the affection of butorphanol on the biological events of CRC cells. To sum up, butorphanol may extenuate the aggressive cellular behaviors to produce tumor-suppressing activity on CRC via binding with SIGMAR1.
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