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ETV2 regulating PHD2-HIF-1α axis controls metabolism reprogramming promotes vascularized bone regeneration

Bioactive Materials 2024年第7期37卷 222-238页

作者： HaoRan Du Bang Li Rui Yu Xiaoxuan Lu ChengLin Li HuiHui Zhang Fan Yang RongQuan Zhao WeiMin Bao Xuan Yin YuanYin Wang Jian Zhou Jianguang Xu College&Hospital of Stomatology Anhui Medical UniversityKey Lab.of Oral Diseases Research of Anhui ProvinceHefei230032China Salivary Gland Disease Center and Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction Beijing Laboratory of Oral Health and Beijing Stomatological HospitalCapital Medical UniversityBeijing100050China Department of VIP Dental Service School of StomatologyCapital Medical UniversityBeijing100050China Laboratory for Oral and General Health Integration and Translation Beijing Tiantan HospitalCapital Medical UniversityBeijingChina

The synchronized development of mineralized bone and blood vessels is a fundamental requirement for successful bone tissue *** energy production forms the cornerstone supporting new bone *** variant 2(ETV2)has been identified as a transcription factor that promotes energy metabolism reprogramming and facilitates the coordination between osteogenesis and *** vitro molecular experiments have demonstrated that ETV2 enhances osteogenic differentiation of dental pulp stem cells(DPSCs)by regulating the ETV2-prolyl hydroxylase 2(PHD2)-hypoxia-inducible factor-1α(HIF-1α)-vascular endothelial growth factor A(VEGFA)***,ETV2 achieves the rapid reprogramming of energy metabolism by simultaneously accelerating mitochondrial aerobic respiration and glycolysis,thus fulfilling the energy requirements essential to expedite osteogenic ***,decreasedα-ketoglutarate release from ETV2-modified DPSCs contributes to microcirculation ***,we engineered hydroxyapatite/chitosan microspheres(HA/CS MS)with biomimetic nanostructures to facilitate multiple ETV2-DPSC functions and further enhanced the osteogenic *** experiments have validated the synergistic effect of ETV2-modified DPSCs and HA/CS MS in promoting the critical-size bone defect *** summary,this study offers a novel treatment approach for vascularized bone tissue regeneration that relies on energy metabolism activation and the maintenance of a stable local hypoxia signaling state.

关键词： Vascularized bone regeneration ETV2 Hypoxia-inducible factor-1α metabolism reprogramming Microsphere

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m^(6)A-mediated regulation of PBX1-GCH1 axis promotes gastric cancer proliferation and metastasis by elevating tetrahydrobiopterin levels

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Cancer Communications 2022年第4期42卷 327-344页

作者： Yinan Liu Ertao Zhai Junting Chen Yan Qian Risheng Zhao Yan Ma Jianqiu Liu Zhixin Huang Shirong Cai Jianhui Chen Division of Gastrointestinal Surgery Center the First Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Gastric Cancer Center Sun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China Laboratory of Surgery the First Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdong 510080P.R.China

Background:Methyltransferase 3(METTL3)-mediated N6-methyladenosine(m^(6)A)RNA modification has been demonstrated to be a potential factor in promoting gastric cancer(GC).METTL3 regulates a series of signaling pathways by modifying various *** study aimed to identify novel METTL3-mediated signaling pathways and explored possible targets for use in the clinical setting of gastric ***:To investigate the proliferation and metastatic capacity ofGCcell lines with METTL3 knockdown,a xenograft,lung metastasis,and popliteal lymph node metastasis model was ***^(6)A-modified RNA immunoprecipitation(Me-RIP)sequence was utilized to explore the target mRNAs of *** counting kit 8 and transwell assays were performed to investigate the promoting function of pre-B cell leukemia homeobox 1(PBX1)and GTP cyclohydrolase 1(GCH1).Western blotting and chromatin immunoprecipitation were employed to confirm the involvement of the METTL3-PBX1-GCH1 *** and liquid chromatography-mass spectrometry were used to explore the biological function of tetrahydrobiopterin(BH_(4)).Results:Knockdown of METTL3 suppressed xenograft tumor growth and lung/lymph node metastasis in ***,we found that METTL3 combined with and stabilized PBX1 *** immunoprecipitation(ChIP)and further experiments suggested that PBX1 acted as a transcription factor inducing GCH1 ***,the METTL3-PBX1-GCH1 axis increased BH_(4)levels in GC cells,thereby promoting tumor ***:This study suggested that METTL3 enzymes promote tumor growth and lung/lymph node metastasis via METTL3-PBX1-GCH1 axis increasing BH_(4)levels in GC.

关键词： BH_(4) gastric cancer GCH1 m^(6)A metabolism reprogramming metastasis METTL3 PBX1 proliferation

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PNPLA8是调控三阴性乳腺癌磷脂代谢并促进肿瘤增殖和转移的关键分子（英文）

PNPLA8是调控三阴性乳腺癌磷脂代谢并促进肿瘤增殖和转移的关键分...

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2024中国肿瘤标志物学术大会暨CACA整合肿瘤学高峰论坛暨第十七届肿瘤标志物青年科学家论坛暨中国肿瘤标志物产业创新大会

作者：谭哲琼 Pragney Deme Keerti Boyapati Annet A.M.Duivenvoorden Ron M.A.Heeren Caitlin M.Tressler Norman James Haughey Kristine Glunde

Background Triple-negative breast cancer(TNBC) is the most aggressive breast cancer subtype and leads to the poorest patient outcomes despite surgery and chemotherapy treatment. Exploring new molecular mechanisms of TNBC that could lead to the development of novel molecular targets are critically important for improving therapeutic options for treating *** We sought to identify novel therapeutic targets in TNBC by combining genomic and functional studies with lipidomic analysis, which included mechanistic studies to elucidate the pathways that tie lipid profile to critical cancer cell properties. Our studies were performed in a large panel of human breast cancer cell lines and patient *** Comprehensive lipid profiling revealed that phospholipid metabolism is reprogrammed in TNBC cells. We discovered that patatin-like phospholipase domain-containing lipase 8(PNPLA8)is overexpressed in TNBC cell lines and tissues from breast cancer patients. Silencing of PNPLA8disrupted phospholipid metabolic reprogramming in TNBC, particularly affecting the levels of phosphatidylglycerol(PG), phosphatidylcholine(PC), lysophosphatidylcholine(LPC) and glycerophosphocholine(GPC). We showed that PNPLA8 is essential in regulating cell viability,migration and antioxidation in TNBC cells and promoted arachidonic acid and eicosanoid production, which in turn activated PI3K/Akt/Gsk3β and MAPK *** Our study highlights PNPLA8 as key regulator of phospholipid metabolic reprogramming and malignant phenotypes in TNBC, which could be further developed as a novel molecular treatment target.

关键词： PNPLA8 Breast cancer Triple negative Phospholipid metabolism reprogramming Eicosanoids Migration Invasion Proliferation

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