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3-Hydroxyanthranilic acid suppresses colorectal cancer growth and enhances 5-fluorouracil sensitivity via the YY1–p53 and YY1–DKK4 axes [RNA-Seq 3HAA_5FU_HCT116]

ABSTRACT: In spite of its reported tumor-growth-inhibition activity, the role of the tryptophan metabolite 3-hydroxyanthranilic acid (3-HAA) in colorectal cancer (CRC) remains unclear. Here, 3-HAA exhibited depleted levels in CRC tissues, and its exogenous administration effectively suppressed the proliferation of multiple CRC cell lines. Through its binding to the Yin Yang 1 (YY1) transcription factor, it disrupted the YY1–p53 interaction, preserved p53 stability, and induced cell cycle arrest. Notably, in vitro, 3-HAA reduced chemoresistance to the common CRC-chemotherapy drug 5-fluorouracil (5-FU) via the YY1–DKK4 axis. Consistently, in vivo, combined 3-HAA–5-FU treatment effectively inhibited CRC progression, highlighting the potential of 3-HAA for CRC therapy.

ORGANISM(S): Homo sapiens

PROVIDER: GSE338053 | GEO | 2026/09/11

REPOSITORIES: GEO

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3-Hydroxyanthranilic acid suppresses colorectal cancer growth and enhances 5-fluorouracil sensitivity via the YY1-p53 and YY1-DKK4 axes [RNA-Seq 3HAA_HCT116]

Project description:In spite of its reported tumor-growth-inhibition activity, the role of the tryptophan metabolite 3-hydroxyanthranilic acid (3-HAA) in colorectal cancer (CRC) remains unclear. Here, 3-HAA exhibited depleted levels in CRC tissues, and its exogenous administration effectively suppressed the proliferation of multiple CRC cell lines. Through its binding to the Yin Yang 1 (YY1) transcription factor, it disrupted the YY1–p53 interaction, preserved p53 stability, and induced cell cycle arrest. Notably, in vitro, 3-HAA reduced chemoresistance to the common CRC-chemotherapy drug 5-fluorouracil (5-FU) via the YY1–DKK4 axis. Consistently, in vivo, combined 3-HAA–5-FU treatment effectively inhibited CRC progression, highlighting the potential of 3-HAA for CRC therapy.

2026-09-11 | GSE338052 | GEO

3-Hydroxyanthranilic acid suppresses colorectal cancer growth and enhances 5-fluorouracil sensitivity via the YY1-p53 and YY1-DKK4 axes [RNA-Seq 3HAA_HCT116]

Project description:3-Hydroxyanthranilic acid suppresses colorectal cancer growth and enhances 5-fluorouracil sensitivity via the YY1-p53 and YY1-DKK4 axes [RNA-Seq 3HAA_HCT116]

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3-Hydroxyanthranilic acid suppresses colorectal cancer growth and enhances 5-fluorouracil sensitivity via the YY1–p53 and YY1–DKK4 axes [RNA-Seq 3HAA_5FU_HCT116]

Project description:3-Hydroxyanthranilic acid suppresses colorectal cancer growth and enhances 5-fluorouracil sensitivity via the YY1–p53 and YY1–DKK4 axes [RNA-Seq 3HAA_5FU_HCT116]

| PRJNA1492166 | ENA

Leishmania regulates host YY1: comparative proteomic analysis identifies infection modulated YY1 dependent proteinsLeishmania regulates host YY1: comparative proteomic analysis identifies infection modulated YY1 dependent proteins

Project description:The protein Yin-Yang 1 (YY1) is a ubiquitous multifunctional transcription factor. Interestingly, there are several cellular functions controlled by YY1 that could play a role in Leishmania pathogenesis. Leishmaniasis is a human disease caused by protozoan parasites of the genus Leishmania. This study examined the potential role of macrophage YY1 in promoting Leishmania intracellular survival. Knockdown of YY1 resulted in attenuated survival of Leishmania in infected macrophages, suggesting a role of YY1 in Leishmania persistence. Biochemical fractionation studies revealed Leishmania infection caused redistribution of YY1 to the cytoplasm from the nucleus where it is primarily located. Inhibition of nuclear transport by leptomycin B attenuates infection-mediated YY1 redistribution and reduces Leishmania survival. This suggests that Leishmania induces the translocation of YY1 from the nucleus to the cytoplasm of infected cells, where it may regulate host molecules to favour parasite survival. A label-free quantitative whole proteome approach showed that the expression of a large number of macrophage proteins was dependent on the YY1 level. Interestingly, several of these proteins were modulated in Leishmania-infected cells, revealing YY1-dependent host response and suggesting their potential role in Leishmania pathogenesis. Together, these findings identify YY1 as a novel and essential virulence factor by proxy that promotes Leishmania survival.

2025-03-14 | PXD059968 | Pride

Novel mechanisms of 5-Fluorouracil Resistance in Colorectal Cancer: A Proteomic Investigation

Project description:One of the main obstacles to therapeutic success in colorectal cancer (CRC) is the development of acquired resistance to treatment with drugs such as 5-fluorouracil (5-FU), the most commonly used drug in CRC patients. Whilst some mechanisms of resistance are well-known, it is clear from the stasis in therapy success rate, that much is still unknown. Here a proteomics approach is taken towards identification using 5-FU resistant sublines of human CRC cell lines generated in-house. Using a multiplexed stable isotope labelling with amino acids in cell culture (SILAC) proteomics strategy, the resistant cell lines, and equivalently passaged 5-FU-sensitive cell lines were compared to parent cell lines grown in Heavy medium using 2D liquid chromatography and Orbitrap Fusion™ Tribrid™ Mass Spectrometry analysis.

2024-06-16 | PXD047672 | Pride

The post-translational modifications and translation-regulatory role of METTL14 in 5-fluorouracil-resistant colorectal cancer [Ribo-seq]

Project description:5-fluorouracil (5‑FU) based chemotherapy is the first-line chemotherapy scheme for CRC, whereas acquired drug resistance poses a huge obstacle to curing CRC patients and the mechanism is still obscure. METTL14 is a core subunit of the m6A methyltransferase complex and has been reported to regulate the drug resistance of cancers. Here, we demonstrated that METTL14 is significantly downregulated in 5-FU-resistant CRC and METTL14 overexpression inhibits the proliferation and 5-FU resistance of CRC cells in vitro and in vivo. In addition, we found that MIB1 catalyzes the K63-linked ubiquitination of METTL14 and induces its degradation through the autolysosome pathway, while AURKA-mediated phosphorylation enhances METTL14 stability by inhibiting its ubiquitination. Moreover, we first discovered that METTL14 functions in 5-FU-resistant CRC cells by directly participating in the translation initiation of non-m6A-modified mRNAs independently of METTL3, rather than cooperating with METTL3 to methylate adenosine residues of targets. Further analysis indicated that METTL14 regulates the cell cycle process in 5-FU-resistant CRC cells. Collectively, our study not only identified METTL14 as a potential therapeutic target for 5-FU resistance in CRC but also revealed a novel translation-facilitating role of METTL14.

2023-12-01 | GSE219172 | GEO

The post-translational modifications and translation-regulatory role of METTL14 in 5-fluorouracil-resistant colorectal cancer [mRNA-seq]

2023-12-01 | GSE219171 | GEO

RNA-Seq profiling of circular RNAs in human colorectal cancer 5-fluorouracil resistance and the potential biomarkers

Project description:Colorectal cancer（CRC）is a commonly diagnosed cancer of the digestive system worldwide. Although chemotherapeutic agents and targeted therapeutic drugs are currently available for CRC treatment, drug resistance is a problem that cannot be ignored and needs to be solved. 5-Fluorouracil (5-Fu) is a first-line chemotherapeutic agent for colorectal cancer, to explore the role of circular RNA (circRNA) in 5-Fu resistance, we performed the circRNA expression profile in two CRC cell lines and their homologous 5-Fu resistant cells by high-throughput sequencing. We validated the differentially expressed circRNAs in other two paired CRC cells, confirmed that circ_0002813 and circ_0000236 could have a potential ceRNA mechanism and be involved in the formation of 5-Fu resistance. And we combined the sequencing results of mRNA to construct the regulatory network of circRNA-miRNA-mRNA. Our study revealed that circ_0002813 and circ_0000236 may as the biomarkers to predict the occurrence of 5-Fu resistance in CRC.

2024-08-05 | GSE181537 | GEO

Aptamer-modified 5-fluorouracil encapsulated metal-organic framework nanodrugs for enhanced therapy of colorectal cancer via peroxidative induced cell death

Project description:Colorectal cancer (CRC) remains one of the most devastating malignancies worldwide. 5-Fluorouracil (5-FU) is a widely used therapeutic agent in CRC treatment. Here, we report a PTK-7–targeted, MOF-based nanodrug (AFZC) comprising Sgc8 aptamer, 5-FU, and Cu-doped ZIF-8. AFZC was synthesized via stepwise loading and surface functionalization and rigorously characterized by SEM/TEM. Targeting specificity was confirmed in PTK-7–positive colorectal cancer cells: Cy5-Sgc8 showed strong internalization in CRC cells but negligible uptake in normal epithelial cells. Functionally, AFZC suppressed proliferation and lowered 5-FU IC₅₀ across multiple CRC lines, with enhanced apoptosis versus 5-FU alone. Patient-derived organoids demonstrated greater growth inhibition with AFZC than with 5-FU. Transcriptomic profiling of AFZC-treated CRC cells highlighted pro-apoptotic remodeling with upregulation of NECTIN4 and NCF2, and concordant increases by Western blot alongside caspase cleavage. In vivo, AFZC achieved superior tumor control over 5-FU or ZIF-8 in CRC xenografts and a PDX model. No toxicity was found in histopathology of major organs or in liver/renal function markers at the treatment dosage. Collectively, AFZC couples selective PTK-7 targeting, catalytic activity, and sustained drug release to potentiate 5-FU efficacy with a favorable toxicity profile, supporting its translational promise in CRC.

2026-01-06 | GSE315569 | GEO

Synergistic effects of 5-Fluorouracil in combination with Salinomycin promoted ferroptosis via inhibiting SLC7A11/GPX4 in Colorectal Cancer

Project description:5-FU resistance is considered to be a possible reason for the failure of conventional drug treatment of colorectal cancer (CRC). Recently, salinomycin (SAL), as a selective inhibitor of cancer stem cells (CSCs), has been used to sensitize and attenuate a variety of solid tumor chemotherapy drugs. In our study, our goal was to combine SAL with 5-FU to explore whether increase the sensitivity of CRC to 5-FU and the molecular mechanism that involved in enhancing 5-FU sensitivity and promoting tumor cell chemotherapeutic death.

2025-06-10 | GSE298808 | GEO

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