Yuheng Pang

Beijing YouAn Hospital

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Liujia Chan

Beijing YouAn Hospital

Yuji Wang

Huazhong University of Science and Technology

Wenjing Wang

National University of Singapore

Jizong Zhao

Beijing Tian Tan Hospital

Peicong Ge

National Clinical Research Center for Digestive Diseases

Qian Zhang

Beijing Tian Tan Hospital

Junsheng Li

Capital Medical University

Qiheng He

National Clinical Research Center for Digestive Diseases

Wenjing Wang

Guangzhou University of Chinese Medicine

Zhikang Zhao

Beijing Tian Tan Hospital

Cooperative Institutions

Capital Medical University

Beijing Tian Tan Hospital

National Clinical Research Center for Digestive Diseases

Harbin Medical University

Third Affiliated Hospital of Harbin Medical University

Beijing YouAn Hospital

Chinese Institute for Brain Research

Peking University

Sichuan University

Chinese Academy of Medical Sciences & Peking Union Medical College

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T Cells Immune Imbalance Present in Patients With Multiple Intracranial Aneurysms

Clinical & Experimental Immunology (2024)

Chuming Tao Chenglong Liu Peicong Ge Liujia Chan Yuheng Pang

Growing evidence suggests that systemic immune and inflammatory responses may play a critical role in the formation and development of aneurysms. Exploring the differences between single intracranial aneurysm (SIA) and multiple IAs (MIAs) could provide insights for targeted therapies. However, there is a lack of comprehensive and detailed characterization of changes in circulating immune cells in MIAs. Peripheral blood mononuclear cell (PBMC) samples from patients with SIA (n = 16) or MIAs (n = 6) were analyzed using high-dimensional mass cytometry to evaluate the frequency and phenotype of immune cell subtypes. A total of 25 cell clusters were identified, revealing that the immune signature of MIAs included cluster changes. Compared to patients with SIA, patients with MIAs exhibited immune dysfunction and regulatory imbalance in T-cell clusters. They also had reduced numbers of CD8+ T cells and their subgroups CD8+ Te and CD8+ Tem cells, as well as reduced numbers of the CD4+ T-cell subgroup CD27-CD4+ Tem cells. Furthermore, compared to SIA, MIAs were associated with enhanced T-cell immune activation, with elevated expression levels of CD3, CD25, CD27, CCR7, GP130, and interleukin 10. This study provides insights into the circulating immune cell profiles in patients with MIAs, highlighting the similarities and differences between patients with SIA and those with MIAs. Furthermore, the study suggests that circulating immune dysfunction may contribute to development of MIAs.

10.1093/cei/uxae058

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Innate Immune Cell Profiling in Peripheral Blood Mononuclear Cells of Patients with Moyamoya Disease

Inflammation (2024)

Chenglong Liu Siqi Mou Bojian Zhang Yuheng Pang Liujia Chan

Moyamoya Disease

Monocyte

10.1007/s10753-024-02201-4

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Citations (1)

High-Dimensional Immune Profiling by Mass Cytometry Revealed the Circulating Immune Cell Landscape in Patients With Intracranial Aneurysm

Frontiers in Immunology (2022)

Peicong Ge Chenglong Liu Liujia Chan Yuheng Pang Hao Li

Increasing evidence supports a critical role of chronic inflammation in intracranial aneurysm (IA). Understanding how the immunological alterations in IA provides opportunities for targeted treatment. However, there is a lack of comprehensive and detailed characterization of the changes in circulating immune cells in IA.To perform a comprehensive and detailed characterization of the changes in circulating immune cells in patients with IA.Peripheral blood mononuclear cell samples from IA patients (n = 26) and age-and sex-matched healthy controls (HCs, n = 20) were analyzed using high dimensional mass cytometry, and the frequency and phenotype of immune cell subtypes were assessed.We identified 28 cell clusters and found that the immune signature of IA consists of cluster changes. IA patients exhibited dysfunction of immunity, with dysregulation of CD4+ T-cell clusters, increased B cells and monocytes, and decreased CD8+ T cells, DNT cells, and DPT cells. Moreover, compared with findings in HC, IA was associated with enhanced lymphocyte and monocyte immune activation, with a higher expression of HLA-DR, CXCR3, and CX3CR1. In addition, the expression of TLR4, p-STAT3, and the exhaustion marker PD1 was increased in T cells, B cells, and NK cells in IA patients.Our data provide an overview of the circulating immune cell landscape of IA patients, and reveal that the dysfunction of circulating immunity may play a potential role in the development of IA.

Mass cytometry

CXCR3

10.3389/fimmu.2022.922000

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Highly-tumor-targeted PAD4 inhibitors with PBA modification inhibit tumors in vivo by specifically inhibiting the PAD4-H3cit-NETs pathway in neutrophils

European Journal of Medicinal Chemistry (2023)

Di Zhu Lu Yu Bo Hu Yuheng Pang Bingru Liu

10.1016/j.ejmech.2023.115619

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Mitosis targeting in non-small lung cancer cells by inhibition of PAD4

Heliyon (2024)

Xiangmei Wu Liujia Chan Di Zhu Yuheng Pang Mulan Jin

PAD4 expression and activity were significantly up-regulated in lung cancer tissues suggesting that PAD4 could be a possible target for lung cancer treatment. In this study we had demonstrated that PAD4 expression was higher in lung cancer patients whom with lymphnode metastasis and pleural invasion. Inhibiting PAD4 with a small molecular inhibitor could induce apoptosis and suppress growth in lung cancer cells. We used RNA-sequencing to further investigate transcriptional changes that induced by PAD4 inhibition, and results suggested its affected mostly on the cell cycle, mitotic cell cycle process, p53 signaling pathway. By using image flow cytometry analysis, we found that PAD4 inhibited by YW3-56 could accumulate cells in the G1/G0 phases and reducing the fraction of G2/M and S phase cells. Quantification of different phase of mitosis in cells treated with YW3-56 revealed an increasing trend of telophase and prophase cells. Taken together, our data indicated that PAD4 inhibitor could affect cell cycle and mitosis of lung cancer cells, and targeting PAD4 could be a promising strategy for discovery novel anti-NSCLC treatments.

10.1016/j.heliyon.2024.e27313

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Citations (1)

Rosmarinic acid promotes mitochondrial fission and induces ferroptosis in triple-negative breast cancer cells

Naunyn-Schmiedeberg s Archives of Pharmacology (2025)

Chufei Xie Liujia Chan Yuheng Pang Yuefeng Shang Wenjing Wang

Triple-negative breast cancer

Rosmarinic acid

10.1007/s00210-025-03927-0

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Cancer stem cells promote lymph nodes metastasis of breast cancer by reprogramming tumor microenvironment

Translational Oncology (2023)

Lin Li Jianyu Liu Wenzheng Wang Yingqiang Fu Yuhan Deng

Breast cancer progression and metastasis are governed by a complex interplay within the tumor immune microenvironment (TIME), involving numerous cell types. Lymph node metastasis (LNM) is a key prognostic marker associated with distant organ metastasis and reduced patient survival, but the mechanisms underlying its promotion by breast cancer stem cells (CSCs) remain unclear. Our study sought to unravel how CSCs reprogram TIME to facilitate LNM. Utilizing single-cell RNA sequencing, we profiled TIME in primary cancer and corresponding metastatic lymph node samples from patients at our institution. To verify the derived data, we cultured CSCs and performed validation assays employing flow cytometry and CyTOF. Our analysis revealed distinct differences in cellular infiltration patterns between tumor and LNM samples. Importantly, RAC2 and PTTG1 double-positive CSCs, which exhibit the highest stem-like attributes, were markedly enriched in metastatic lymph nodes. These CSCs are hypothesized to foster metastasis via activation of specific metastasis-related transcription factors and signaling pathways. Additionally, our data suggest that CSCs might modulate adaptive and innate immune cell evolution, thereby further contributing to metastasis. In summary, this study illuminates a critical role of CSCs in modifying TIME to facilitate LNM. The enrichment of highly stem-like CSCs in metastatic lymph nodes offers novel therapeutic targeting opportunities and deepens our understanding of breast cancer metastasis.

Reprogramming

10.1016/j.tranon.2023.101733

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Targeting mitochondrial dynamics by AZD5363 in triple-negative breast cancer MDA-MB-231 cell–derived spheres

Naunyn-Schmiedeberg s Archives of Pharmacology (2023)

Yingqiang Fu Wei Dong Yuting Xu Lin Li Yu Xin

Breast cancer stem cells (BCSCs) have been suggested to contribute to chemotherapeutic resistance and disease relapse in breast cancer. Thus, BCSCs represent a promising target in developing novel breast cancer treatment strategies. Mitochondrial dynamics in BCSCs were recently highlighted as an available approach for targeting BCSCs. In this study, a three-dimensional (3D) cultured breast cancer stem cell spheres model was constructed. Mitochondrial dynamics and functions were analyzed by flow cytometry and confocal microscopy. We have demonstrated that the protein levels of FIS 1 and Mitofusin 1 were significantly increased in BCSCs. Moreover, Capivasertib (AZD5363) administration could suppress Mitofusin1 expression in BCSCs. Our use of MitoTracker Orange and annexin V double-staining assay suggested that AZD5363 could induce apoptosis in BCSCs. The sensitivity of stem cell spheres to doxorubicin was investigated by CCK8 assay, and our results indicated that AZD5363 could re-sensitize BCSCs to Doxo. Flow cytometry analysis identified doxo-induced CD44 and CD133 expression in BCSCs could be suppressed by AZD5363. In combination with AZD536, doxo-induced apoptosis in the BCSCs was significantly increased. In conclusion, our study explored, for the first time, that AZD5363 could target mitochondrial dynamics in 3D cultured stem cell spheres (BCSCs) by regulating Mitofusin.

10.1007/s00210-023-02477-7

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Citations (6)

The hepatitis B virus promotes the progression of non-alcoholic fatty liver disease through incomplete autophagy

Free Radical Biology and Medicine (2023)

Yang Wang Jiaxi Li Shanshan Wang Yuheng Pang Pengxiang Liu

Lipid droplet

Steatosis

Liver disease

Pathogenesis

10.1016/j.freeradbiomed.2023.05.020

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Citations (5)

The combination of the HDAC1 inhibitor SAHA and doxorubicin has synergic efficacy in triple negative breast cancer in vivo

Pharmacological Research (2023)

Yuheng Pang Runze Shi Liujia Chan Lu Yu Di Zhu

Vorinostat (SAHA) is a histone deacetylase inhibitor that exerts its effects through epigenetic regulation. Specifically, SAHA can inhibit the proliferation of triple-negative breast cancer (TNBC) cells alone or in combination with other chemotherapeutic agents. Doxorubicin (DOX), a traditional chemotherapeutic drug, exhibits a potent cytotoxic effect on cancer cells while also inducing strong toxic effects. In this study, we investigated the synergistic potential of these two drugs in combination against TNBC. Our results suggested that the combination of these two drugs could enhance the inhibitory effect on cancer cell proliferation, resulting in alterations in cell mitotic phase, and suppression of cancer cell stemness. Moreover, our in vivo study unveiled that when SAHA was combined with DOX, it not only exhibited an inhibitory effect on tumor metastasis but also played a role in regulating the immune microenvironment within tumors. Overall, the combination of DOX and SAHA presents a promising avenue for innovative combination chemotherapy in the context of TNBC.

Triple-negative breast cancer

Vorinostat

Histone deacetylase inhibitor

HDAC1

10.1016/j.phrs.2023.106926

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Citations (7)