ArticleTranslational cancer research2020
FAM172A affects cell proliferation and apoptosis not by targeting β-tubulin in HepG2 cells.
Article in Translational cancer research, 2020. 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
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, 3 citations in OpenAlex.
- FAM172A promotes epithelial ovarian cancer progression and induces platinum resistance via the PI3K/AKT pathway.Scientific reports · 2025Article
- mInternational journal of oncology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMicrotubules pull chromosomes apart during cell mitosis and take part in cell division, Inhibiting the formation of spindle microtubules during mitosis has become one of the current anti-tumor research strategies. Earlier studies have found that the family with sequence similarity 172, member A (FAM172A) can significantly inhibit the proliferation of human colorectal cancer cell line LOVO cells and promote apoptosis. The purpose of this study was to investigate the biological effects of FAM172A on liver cancer cells and the interaction mechanism with tubulin.
methodsUse STRING software predicted the interactions between FAM172A and β-tubulin, and verify by immunoprecipitation. Real-Time qPCR was used to determine the expression levels of β-tubulin in liver cancer cell line HepG2, western blot was performed to detect protein expression levels. Immunofluorescence experiment to detect the distribution, shape and the dynamic behavior of depolymerization-aggregation of β-tubulin in cells. MTT, wound healing and Transwell assay were employed to determine cell proliferation, migration and invasion respectively. Flow cytometry was conducted to determine cell cycle and apoptosis.
resultsThere is no interactions between FAM172A and β-tubulin. We determined that when FAM172A was up-regulated or down-regulated, the mRNA and protein levels of β-tubulin did not change significantly (P>0.05). Furthermore, the distribution, shape of β-tubulin in cells, and the dynamic behavior of depolymerization-aggregation was not affected. After FAM172A overexpression, the migration and invasion of HepG2 cells were significantly inhibited (P<0.05), the cell proliferation was also significantly inhibited (P<0.05) and was time-dependent. The HepG2 cells had apparent S phase arrest and apoptosis (P<0.05). After interfering with FAM172A, the opposite result will appear.
conclusionsThe results show that FAM172A may be a new tumor suppressor gene, which has a specific role in cell cycle control and cell proliferation, but the specific mechanism of action has not been explained in this study and needs further exploration.
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.