ArticleMolecular cancer2019
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Article in Molecular cancer, 2019. 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 It has been retracted, and should not be counted.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 80 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
80 citing papers in PubMed, 158 citations in OpenAlex.
- METTL3: a multifunctional regulator in diseases.Molecular and cellular biochemistry · 2025Review
- RNA mCell investigation · 2025Article
- Pan-cancer analysis reveal that mDiscover oncology · 2025Article
- METTL14 attenuates cancer stemness by suppressing ATF5/WDR74/β-catenin axis in gastric cancer.Cancer science · 2025Article
- Dynamic RNA methylation modifications and their regulatory role in mammalian development and diseases.Science China. Life sciences · 2024Review
- N6-methyladenosine RNA modifications: a potential therapeutic target for AML.Annals of hematology · 2024Review
- Ramifications of m6A Modification on ncRNAs in Cancer.Current genomics · 2024Review
- Targeting key RNA methylation enzymes to improve the outcome of colorectal cancer chemotherapy (Review).International journal of oncology · 2024Review
- The role of the methyltransferase METTL3 in prostate cancer: a potential therapeutic target.BMC cancer · 2024Review
- The two-faced role of RNA methyltransferase METTL3 on cellular response to cisplatin in head and neck squamous cell carcinomaFrontiers in oncology · 2024Article
- The role of m6A epigenetic modifications in tumor coding and non-coding RNA processing.Cell communication and signaling : CCS · 2023Review
- TRIM28 suppresses cancer stem-like characteristics in gastric cancer cells through Wnt/β-catenin signaling pathways.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- N6-methyladenosine (m6A) Modification in Preeclampsia.Reproductive sciences (Thousand Oaks, Calif.) · 2023Review
- Understanding crosstalk of organ tropism, tumor microenvironment and noncoding RNAs in breast cancer metastasis.Molecular biology reports · 2023Review
- TRIM28 recruits E2F1 to regulate CBX8-mediated cell proliferation and tumor metastasis of ovarian cancer.Human cell · 2023Article
- METTL3 promotes proliferation and migration of colorectal cancer cells by increasing SNHG1 stability.Molecular medicine reports · 2023Article
- The roles and implications of RNA mNature reviews. Clinical oncology · 2023Review
- A risk model constructed using 14 NJournal of gastrointestinal oncology · 2023Article
- RNA N6-methyladenosine modification in regulating cancer stem cells and tumor immune microenvironment and its implication for cancer therapy.Journal of cancer research and clinical oncology · 2023Review
- RNA methylation and cellular response to oxidative stress-promoting anticancer agents.Cell cycle (Georgetown, Tex.) · 2023Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
- Retraction · 2023-10-06Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Duplication · Unreliable Data ·
- Retracted
Authors and funding
8 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColon cancer (CC) cells can exhibit stemness and expansion capabilities, which contribute to resistance to conventional chemotherapies. Aberrant expression of CBX8 has been identified in many types of cancer, but the cause of this aberrant CBX8 expression and whether CBX8 is associated with stemness properties in CC remain unknown.
methodsqRT-PCR and IHC were applied to examine CBX8 levels in normal and chemoresistant CC tissues. Cancer cell stemness and chemosensitivity were evaluated by spheroid formation, colony formation, Western blot and flow cytometry assays. RNA-seq combined with ChIP-seq was used to identify target genes, and ChIP, IP and dual luciferase reporter assays were applied to explore the underlying mechanisms.
resultsCBX8 was significantly overexpressed in chemoresistant CC tissues. In addition, CBX8 could promote stemness and suppress chemosensitivity through LGR5. Mechanistic studies revealed that CBX8 activate the transcription of LGR5 in a noncanonical manner with assistance of Pol II. CBX8 recruited KMT2b to the LGR5 promoter, which maintained H3K4me3 status to promote LGR5 expression. Moreover, m
conclusionsUpon m
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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.