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Received β€” 27 May 2026 ⏭

PRXL2B facilitates the progression of hepatocellular carcinoma and the therapeutic efficacy of oncolytic adenovirus H101 through the PI3K/AKT/PD-L1 axis

βœ‡Omics in Hepatocellular
By: Ziqi Zhang Β· Hongli Chen Β· Yangming Liu Β· Hao Wang Β· You Yan Β· Yanxi Yu Β· Zuotian Huang Β· Yanyao Liu Β· Wei Li Β· Zhongjun Wu Β· Meiqing Kang Β· Xiaoyong Luo Β· Ping Che Β· Rui Liao
20 May 2026 at 18:00

Biosci Trends. 2026 May 21. doi: 10.5582/bst.2026.01000. Online ahead of print.

ABSTRACT

Oncolytic adenovirus H101 has shown antitumor activity in hepatocellular carcinoma (HCC), but the molecular determinants of treatment response remain unclear. In this study, a Hepa1-6 subcutaneous tumor model was established in C57BL/6 mice and treated with intratumoral H101, followed by integrated transcriptomic and proteomic analyses to identify candidate genes associated with H101 response. PRXL2B was selected for further investigation using public multi-omics datasets, tissue microarray-based immunohistochemistry, in vitro functional assays, mechanistic analyses, and in vivo validation experiments. Integrated multi-omics analyses identified PRXL2B as a candidate gene downregulated after H101 treatment. Public datasets and tissue-based validation further showed that PRXL2B was upregulated in HCC tissues. In MHCC97H and HCCLM3 cells, PRXL2B knockdown inhibited proliferation, migration, and invasion, promoted apoptosis and cell-cycle arrest, and enhanced the antitumor effect of H101. Mechanistically, PRXL2B silencing reduced AKT phosphorylation and PD-L1 expression. In vivo, PRXL2B knockdown suppressed tumor growth, and the combination of PRXL2B knockdown and H101 produced the strongest antitumor effect. These findings indicate that PRXL2B promotes malignant phenotypes in HCC and may modulate H101 efficacy through the PI3K/AKT/PD-L1 axis. Targeting PRXL2B may therefore represent a potential strategy to enhance the therapeutic efficacy of oncolytic virus therapy in HCC.

PMID:42161529 | DOI:10.5582/bst.2026.01000

Received β€” 17 March 2026 ⏭

LightMoE: Reducing Mixture-of-Experts Redundancy through Expert Replacing

βœ‡cs.AI, q-bio.NC updates on arXiv.org
By: Jiawei Hao Β· Zhiwei Hao Β· Jianyuan Guo Β· Li Shen Β· Yong Luo Β· Han Hu Β· Dan Zeng
16 March 2026 at 12:00
arXiv:2603.12645v1 Announce Type: cross Abstract: Mixture-of-Experts (MoE) based Large Language Models (LLMs) have demonstrated impressive performance and computational efficiency. However, their deployment is often constrained by substantial memory demands, primarily due to the need to load numerous expert modules. While existing expert compression techniques like pruning or merging attempt to mitigate this, they often suffer from irreversible knowledge loss or high training overhead. In this paper, we propose a novel expert compression paradigm termed expert replacing, which replaces redundant experts with parameter-efficient modules and recovers their capabilities with low training costs. We find that even a straightforward baseline of this paradigm yields promising performance. Building on this foundation, we introduce LightMoE, a framework that enhances the paradigm by introducing adaptive expert selection, hierarchical expert construction, and an annealed recovery strategy. Experimental results show that LightMoE matches the performance of LoRA fine-tuning at a 30% compression ratio. Even under a more aggressive 50% compression rate, it outperforms existing methods and achieves average performance improvements of 5.6% across five diverse tasks. These findings demonstrate that LightMoE strikes a superior balance among memory efficiency, training efficiency, and model performance.
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