ArticleComputational and mathematical methods in medicine2022
The Roles of KIFC1 in the Development of Osteosarcoma: Characterization of Potential Therapeutic Targets.
Article in Computational and mathematical methods in medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 2 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
2 citing papers in PubMed, 2 citations in OpenAlex.
- KLC3 activates PI3K/AKT signaling and promotes ovarian cancer cell proliferation and migration through COL3A1.Oncology reports · 2025Article
- RETRACTION: The Roles of KIFC1 in the Development of Osteosarcoma: Characterization of Potential Therapeutic Targets.Computational and mathematical methods in medicine · 2025Article
Corrections and comments
- Retracted
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: As an important member of the mitotic kinesin family, kinesin family member C1 (KIFC1) is abnormally expressed in a variety of tumors. However, the roles of KIFC1 in the development of osteosarcoma (OS) have never been elucidated. Methods: The expression of KIFC1 in OS tissues which was detected by immunohistochemistry (IHC) staining was further confirmed by Gene Expression Profiling Interactive Analysis 2 (GEPIA2) database. The relationship between KIFC1 and CDC20 was analyzed by clinical data, STRING database, and GEPIA2 database. Survival analysis was performed through GEPIA2 database. To elucidate the roles of KIFC1 in OS, MG-63 and U-2 OS cells were treated with short hairpin RNA (shRNA) to knock down KIFC1 expression, and the knockdown efficiency was validated with quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and western blotting (WB). Moreover, colony formation and Cell Counting Kit-8 (CCK-8) assays were utilized to evaluate cell proliferation. Results: According to IHC staining and GEPIA2 analysis, the expression of KIFC1 in OS tissues was significantly higher than that in adjacent normal tissues, which was inversely connected to the prognosis. These results were consistent with our clinical data. Besides, KIFC1 was positively correlated with CDC20. In addition, KIFC1 shRNA could effectively silence KIFC1 expression in MG-63 and U-2 OS cells. Furthermore, the knockdown of KIFC1 inhibited the cell proliferation ability with increased cell apoptosis in MG-63 and U-2 OS cells. Conclusion: KIFC1 was significantly upregulated in OS and promoted OS progression by cell proliferation. These findings offered new clues for OS diagnosis and prognosis, suggesting KIFC1 could be a potential therapeutic target for OS in further study.
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.