Sha Wu

Southern Medical University

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Chenfei Zhou

Shanghai Jiao Tong University

Wei Wang

Huazhong University of Science and Technology

Wenfei Wei

China University of Petroleum, Beijing

Lei Huang

Newcastle University

Luo-Jiao Liang

Nanfang Hospital

Rui-Ming Yan

Southern Medical University

Xiang‐Guang Wu

First Affiliated Hospital of Guangzhou Medical University

Hongyan Yi

Liaoning Technical University

Liangsheng Fan

First Affiliated Hospital of Guangzhou Medical University

Zi‐Ci Wang

Guangzhou Medical University

Cooperative Institutions

Southern Medical University

108

Nanfang Hospital

Huazhong University of Science and Technology

Guangzhou Medical University

Sun Yat-sen University

Chinese Academy of Medical Sciences & Peking Union Medical College

Chinese Academy of Sciences

Sichuan University

Shanghai Jiao Tong University

First Affiliated Hospital of Guangzhou Medical University

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Strategies and Rules for Tuning TCR-derived Therapy

Expert Reviews in Molecular Medicine (2023)

Guoheng Mo Xinyu Lu Sha Wu Wei Zhu

Manipulation of T cells has revolutionized cancer immunotherapy. Notably, the use of T cells carrying engineered T cell receptors (TCR-T) offers a favourable therapeutic pathway, particularly in the treatment of solid tumours. However, major challenges such as limited clinical response efficacy, off-target effects and tumour immunosuppressive microenvironment have hindered the clinical translation of this approach. In this review, we mainly want to guide TCR-T investigators on several major issues they face in the treatment of solid tumours after obtaining specific TCR sequences: (1) whether we have to undergo affinity maturation or not, and what parameter we should use as a criterion for being more effective. (2) What modifications can be added to counteract the tumour inhibitory microenvironment to make our specific T cells to be more effective and what is the safety profile of such modifications? (3) What are the new forms and possibilities for TCR-T cell therapy in the future?

Cancer Immunotherapy

10.1017/erm.2023.27

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Hypoxia-induced ZEB1 promotes cervical cancer progression via CCL8-dependent tumour-associated macrophage recruitment

Cell Death and Disease (2019)

Xiaojing Chen Yuan-Run Deng Zi‐Ci Wang Wenfei Wei Chenfei Zhou

The accumulation of tumour-associated macrophages (TAMs) in the hypoxic tumour microenvironment (TME) is associated with malignant progression in cancer. However, the mechanisms by which the hypoxic TME facilitates TAM infiltration are not fully understood. This study showed that high ZEB1 expression in hypoxic cervical cancer cell islets was positively correlated with CD163

CD163

Hypoxia

Tumor progression

10.1038/s41419-019-1748-1

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Citations (105)

Constitutive signaling from an engineered IL-21 receptor programs long-lived effector TCR-T cells for HCC therapy

Journal of Hepatology (2023)

Wei Pu Zhu Zhiming Zhang Jinzhang Chen Xiaolan Chen Xuan Huang

10.1016/s0168-8278(23)01284-9

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Cervical squamous cell carcinoma-secreted exosomal miR-221-3p promotes lymphangiogenesis and lymphatic metastasis by targeting VASH1

Oncogene (2018)

Chenfei Zhou Jing Ma Lei Huang Hongyan Yi Yanmei Zhang

Cancer-secreted exosomal miRNAs are emerging mediators of cancer-stromal cross-talk in the tumor environment. Our previous miRNAs array of cervical squamous cell carcinoma (CSCC) clinical specimens identified upregulation of miR-221-3p. Here, we show that miR-221-3p is closely correlated with peritumoral lymphangiogenesis and lymph node (LN) metastasis in CSCC. More importantly, miR-221-3p is characteristically enriched in and transferred by CSCC-secreted exosomes into human lymphatic endothelial cells (HLECs) to promote HLECs migration and tube formation in vitro, and facilitate lymphangiogenesis and LN metastasis in vivo according to both gain-of-function and loss-of-function experiments. Furthermore, we identify vasohibin-1 (VASH1) as a novel direct target of miR-221-3p through bioinformatic target prediction and luciferase reporter assay. Re-expression and knockdown of VASH1 could respectively rescue and simulate the effects induced by exosomal miR-221-3p. Importantly, the miR-221-3p-VASH1 axis activates the ERK/AKT pathway in HLECs independent of VEGF-C. Finally, circulating exosomal miR-221-3p levels also have biological function in promoting HLECs sprouting in vitro and are closely associated with tumor miR-221-3p expression, lymphatic VASH1 expression, lymphangiogenesis, and LN metastasis in CSCC patients. In conclusion, CSCC-secreted exosomal miR-221-3p transfers into HLECs to promote lymphangiogenesis and lymphatic metastasis via downregulation of VASH1 and may represent a novel diagnostic biomarker and therapeutic target for metastatic CSCC patients in early stages.

Lymphangiogenesis

Lymphatic Endothelium

10.1038/s41388-018-0511-x

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Citations (185)

Adoptive transfer of GRP78-treated dendritic cells alleviates insulitis in NOD mice

Journal of Leukocyte Biology (2021)

Xiaoqi Zhou Muyang Yang Yibing Lv Heli Li Sha Wu

Abstract The 78-kDa glucose-regulated protein (GRP78) has extracellular, anti-inflammatory properties that can aid resolving inflammation. It has been established previously that GRP78 induced myeloid CD11c+ cell differentiation into distinct tolerogenic cells. This tolerance induction makes GRP78 a potential therapeutic agent for transplanted allogeneic grafts and autoimmune diseases, such as type 1 diabetes. In this research, it is revealed that rmGRP78-treated NOD mice bone marrow-derived CD11c+ cells (GRP78-DCs) highly expressed B7-H4 but down-regulated CD86 and CD40, and retained a tolerogenic signature even after stimulation by LPS. In the assessment of in vivo therapeutic efficacy after the adoptive transfer of GRP78-DCs into NOD mice, fluorescent imaging analyses revealed that the transfer specifically homed in inflamed pancreases, promoting β-cell survival and alleviating insulitis in NOD mice. The adoptive transfer of GRP78-DCs also helped reduce Th1, Th17, and CTL, suppressing inflammatory cytokine production in vivo. The findings suggest that adoptive GRP78-DC transfer is critical to resolving inflammation in NOD mice and may have relevance in a clinical setting.

Adoptive Cell Transfer

Insulitis

NOD mice

CD11c

10.1002/jlb.3ma0921-219rrrr

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Citations (6)

Engineering alpha-fetoprotein to develop vaccines and T cell immunotherapies for hepatocellular carcinoma: From preclinical studies to future perspectives

Yukai He Sha Wu

Alpha-fetoprotein

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Oncogenic viral antigens for engineered T cell immunotherapy: Challenges and opportunities

Medicine Advances (2023)

Haipeng Zhang Jing Chen Qianbing Zhang Lingfeng Yu Xiaohong Li

Abstract Viruses that cause malignancies such as hepatocellular carcinoma and cervical cancer are the cause of approximately 20% of all human cancers. In recent years, engineered T cell immunotherapy targeting tumor‐associated antigens (TAAs) has had some success against virus‐associated cancer, although these treatments are associated with side effects. TAA‐specific‐modified T cells may kill cancer cells but they also react with and damage healthy tissue. During an oncogenic virus infection, viral DNA integrates into the host genome, leading to the expression of viral‐specific antigens in the tumor in a restricted and durable manner. The cross‐reactive side‐effects of conventional TAA‐specific engineered T cell treatment can be avoided by creating engineered T cells that target oncogenic viral antigens. To chart a course for the discovery of additional viral‐specific antigens and their combination with immune checkpoint inhibition therapies, this review summarizes the development, preclinical research, and clinical application of oncogenic viral antigen–specific T cell immunotherapy. This review also addresses challenges such as virus mutation and diverse integration, which can result in the loss of the target.

Cancer Immunotherapy

10.1002/med4.37

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Tumor-secreted exosomal Wnt2B activates fibroblasts to promote cervical cancer progression

Oncogenesis (2021)

Luo-Jiao Liang Yang Yang Wenfei Wei Xiang‐Guang Wu Rui-Ming Yan

Abstract The activation of stromal fibroblasts into cancer-associated fibroblasts (CAFs) has been suggested to promote primary tumor growth and progression; however, the mechanisms underlying the crosstalk between tumors and fibroblasts that drives stromal heterogeneity remain unknown. Here, we show that high Wnt2B levels were positively correlated with the number of CAFs in cervical cancer (CC). More importantly, Wnt2B was characteristically enriched in CC cell-secreted exosomes and transferred into fibroblasts to promote fibroblast activation via Wnt/β-catenin signaling, and inhibiting exosomal release or the Wnt/β-catenin signaling pathway diminished the activation induced by exosomal Wnt2B. Moreover, circulating exosomal Wnt2B also promoted CAF conversion in vitro and its expression was significantly higher in CC patients. In conclusion, our findings indicate that CC cell-derived Wnt2B can induce the activation of fibroblasts into CAFs, mainly via exosome-dependent secretion, thus providing directions for the development of diagnostic and therapeutic targets for CC progression.

Exosome

Cancer-Associated Fibroblasts

Tumor progression

10.1038/s41389-021-00319-w

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Citations (33)

Protective effect of chloral hydrate against lipopolysaccharide/D-galactosamine-induced acute lethal liver injury and zymosan-induced peritonitis in mice

International Immunopharmacology (2010)

Qingjun Pan Yuan Liu Jian Zheng Xiao Lu Sha Wu

Chloral hydrate

Galactosamine

Zymosan