APOC1 promotes the progression of osteosarcoma by binding to MTCH2

Li, Renjie; He, Huixian; He, Xu

doi:10.3892/etm.2023.11862

Cited by 7 publications

(2 citation statements)

References 54 publications

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“…72 Upregulated MTCH2 has also been found in clinical osteosarcoma samples. 73 In osteosarcoma, overexpression of MTCH2 rescues the attenuated cell viability, inhibited proliferation, promoted cell apoptosis, elevated OXPHOS and suppressed the Warburg effect triggered by APOC1 silencing, 74 and the regulation of oncogene FASN on MTCH2 is detected by iTRAQ-based proteomic analysis. 75 On the contrary, upregulation of MTCH2 tends to have a therapeutic effect on thymic squamous cell carcinomas, cervical cancer, colorectal cancer and gastric cancer.…”

Section: Neurodegenerative Diseasesmentioning

confidence: 99%

MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction

Peng,

Yang,

Hou

et al. 2024

DDDT

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Section: Neurodegenerative Diseasesmentioning

confidence: 99%

MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction

Peng,

Yang,

Hou

et al. 2024

DDDT

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“…At present, research suggests that apolipoprotein C1 (APOC1) can affect the metabolism of peripheral lipoproteins [21]. APOC1 is a protein derived from the liver.…”

Section: Introductionmentioning

confidence: 99%

APOC1 reduced anti-PD-1 immunotherapy of nonsmall cell lung cancer via the transformation of M2 into M1 macrophages by ferroptosis by NRF2/HO-1

Mei,

Long,

et al. 2024

Anti-Cancer Drugs

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The treatment strategy for nonsmall cell lung cancer (NSCLC) has always been a hot topic of concern, and its treatment strategies are also emerging. This experiment wants to know the effects of apolipoprotein C1 (APOC1) in immunotherapy of NSCLC. APOC1 mRNA and protein expression were upregulated in lung cancer tissue of patients with NSCLC. programmed cell death protein 1 (PD-1) mRNA expression was negatively correlated with PD-1 mRNA expression in patients. The survival rate of APOC1 high expression was lower than that of low expression in patients with NSCLC. APOC1 gene reduced the transformation of M2 into M1 macrophages (TMMM). APOC1 gene promoted cell growth, and the gene reduced ferroptosis of NSCLC. APOC1-induced nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (NRF2/HO-1) signaling pathway. Sh-APOC1 gene reduced cell growth in mice of NSCLC through the inhibition of NRF2/HO-1 signaling pathway. The inhibition of NRF2 reduced the TMMM by APOC1. The activation of NRF2 reduced the TMMM by si-APOC1. In conclusion, APOC1 reduced anti-PD-1 immunotherapy of NSCLC via the TMMM by ferroptosis by NRF2/HO-1, suggesting that targeting this mechanism of APOC1 may be a feasible strategy for anti-PD-1 immunotherapy for NSCLC.

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M2 macrophage exosome‐derived Apoc1 promotes ferroptosis resistance in osteosarcoma by inhibiting ACSF2 deubiquitination

Yin,

Tang,

Zhao

2024

Molecular Carcinogenesis

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Osteosarcoma (OS) is the most common primary malignant tumor of bone. The aim of this study was to investigate the regulatory mechanisms of M2 macrophage exosomes (M2‐Exos) in ferroptosis in OS. A mouse model was established to investigate the in vivo role of M2‐Exos. We investigated their effects on ferroptosis in OS using erastin, a ferroptosis activator, and deferoxamine mesylate, an iron chelator. In vitro, we investigated whether the Apoc1/Acyl‐CoA Synthetase Family Member 2 (ACSF2) axis mediates these effects, using shApoc1 and shACSF2. The mechanisms whereby Apoc1 regulates ACSF2 were examined using cyclohexanone, a protein synthesis inhibitor, and MG132, a proteasomal inhibitor. M2‐Exos reversed the inhibitory effects of erastin on OS cells, thus enhancing their viability, migration, invasion, proliferation, and reducing ferroptosis. Apoc1 was highly expressed in M2‐Exos, and interfering with this expression reversed the effects of M2‐Exos on OS cells. ACSF2 mediated the effects of M2‐Exos‐derived Apoc1. Apoc1 interacted with ACSF2, which, in turn, interacted with USP40. Apoc1 overexpression increased ACSF2 ubiquitination, promoting its degradation, whereas USP40 overexpression inhibited ACSF2 ubiquitination and promoted its expression. Apoc1 overexpression inhibited ACSF2 binding to USP40. M2‐Exos‐derived Apoc1 promoted ferroptosis resistance by inhibiting USP40 binding to ACSF2 and promoting ACSF2 ubiquitination and degradation, thus enhancing OS development.

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APOC1 promotes the progression of osteosarcoma by binding to MTCH2

Cited by 7 publications

References 54 publications

MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction

MTCH2 in Metabolic Diseases, Neurodegenerative Diseases, Cancers, Embryonic Development and Reproduction

APOC1 reduced anti-PD-1 immunotherapy of nonsmall cell lung cancer via the transformation of M2 into M1 macrophages by ferroptosis by NRF2/HO-1

M2 macrophage exosome‐derived Apoc1 promotes ferroptosis resistance in osteosarcoma by inhibiting ACSF2 deubiquitination

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