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Xuying Huang

As seen in: Nature, MDPI, Molecular Cancer Research
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Articles

Targeting enolase isoenzyme 2 enables precision glycolysis inhibition in VHL -mutant renal cell carcinoma

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By Jiannan Yao, Xiaona Fan, Xichen Dong, Qianqian Sun, Xuying Huang, Heshu Liu, Xiangyu Chen, Yanjun Jia, Haili Qian, Tao Wen, Jian Liu, Huixian Xin, Fuhui Wan
| Nature Verified
Abstract Clear cell renal cell carcinoma (ccRCC) exhibits glycolytic addiction due to VHL mutation, making it vulnerable to metabolic intervention. While conventional inhibitors targeting core housekeeping glycolytic enzymes show robust antitumor efficacy, their clinical use is limited by on-target systemic toxicity. Here, we identify enolase 2 (ENO2) as an isoform-specific glycolytic vulnerability specific to VHL-deficient ccRCC.
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[2510.07028] Temporal-Prior-Guided View Planning for Periodic 3D Plant Reconstruction

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By Xuying Huang, Maren Bennewitz
| arxiv.org
arXiv:2510.07028 (cs) View PDF HTML (experimental) Comments: Subjects: Robotics (cs.RO) Cite as: arXiv:2510.07028 [cs.RO] (or arXiv:2510.07028v1 [cs.RO] for this version) https://doi.org/10.48550/arXiv.2510.07028 Submission history From: Sicong Pan [ view email] [v1] Wed, 8 Oct 2025 13:57:29 UTC (4,624 KB) Bibliographic Tools Bibliographic Explorer Toggle Bibliographic Explorer () Connected Papers Toggle Connected Papers (What is Connected Papers?) Litmaps Toggle Litmaps (What is Litmaps?)...
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Hypoxic stimulation of DCLK1 transcription and alternative-promoter switching fuels tumor malignancy in clear cell renal cell carcinoma - Cell Death & Disease

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By Jiannan Yao, Xuying Huang, Yang Ge, Guangyu An
| Nature Verified
Abstract Alterations in the diversity and abundance of oncogenic gene transcripts are key factors driving tumor initiation and progression. DCLK1, an emerging cancer stem cell marker, is activated during tumorigenesis, triggering cancer stemness and metastasis. It produces long or short isoforms through selective usage of alternative promoters (α- or β-promoter). However, the mechanism mediating DCLK1 activation and choice of AP model in cancer remains unclear.
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