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Published Research PapersFiltered: Year 2026 • Vol 42

Showing 4 of 10 peer-reviewed papers with full Graphical Abstracts.

Original ResearchVol 42, Issue 6 • pp. 100-112DOI: 10.3969/j.issn.1000-4718.2026.06.013• Jan 15, 2026

Enterococcus faecalis Promotes Chemoresistance in Colorectal Cancer via Lactate-Mediated MOB3B Down-Regulation

Authors: QI Jingru, ZHANG Weiyang, YANG Longan, LI Yuxuan, SHI Zhuoran, LIN Chuman, HUANG Yiyan, HUA Xing, ZHOU Rui, YU Lina

AIM: To investigate the role of Enterococcus faecalis (E. faecalis) in colorectal cancer (CRC) chemoresistance and elucidate the underlying molecular mechanisms. METHODS: Conditioned media (CM) were collected from cultures of E. faecalis treated with oxaliplatin or 5-fluorouracil (5-FU). The effects of these media on CRC chemoresistance were evaluated using in vitro functional assays and in vivo xenograft models in nude mice. Bioinformatics analysis was conducted to identify candidate genes associated with E. faecalis-induced chemoresistance. Gain- and loss-of-function experiments were performed to assess the role of MOB3B in regulating CRC cell proliferation and drug sensitivity. RT-qPCR, Western blot, and immunohistochemistry were used to validate the molecular mechanisms involved. Metabolomic profiling identified key metabolites in E. faecalis-oxaliplatin CM, and their roles in drug resistance were also confirmed. RESULTS: Compared with oxaliplatin treatment alone, E. faecalis-oxaliplatin CM significantly promoted CRC cell growth and chemoresistance in vitro (P<0.01). Tumors treated with E. faecalis-oxaliplatin CM exhibited significantly larger volumes and faster growth in vivo (P<0.01). Mechanistically, down-regulation of MOB3B mediated the chemoresistance-promoting effects of E. faecalis-oxaliplatin CM (P<0.01). Overexpression of MOB3B inhibited CRC cell proliferation and enhanced chemosensitivity, whereas MOB3B knockdown produced the opposite effect (P<0.01). Metabolomic analysis revealed elevated lactate levels in the E. faecalis-oxaliplatin CM (P<0.01). Lactate inhibition significantly reduced CRC cell proliferation, reversed chemoresistance, and restored MOB3B expression (P<0.01). CONCLUSION: E. faecalis promotes chemoresistance in CRC through lactate-mediated down-regulation of MOB3B, highlighting MOB3B as a potential therapeutic target for overcoming CRC chemoresistance.

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Original ResearchVol 42, Issue 5 • pp. 100-112DOI: 10.3969/j.issn.1000-4718.2026.05.014• Jan 15, 2026

A Spatial Atlas of Neuroimmune and Epigenetic Microenvironment in Psoriasis

Authors: XIAN Haiyan, DAI Jingfang, WU Minghui, QIU Xinmin, WANG Maojie, ZHANG Ge, LIU Huazhen, CHEN Yonggen, ZHU Ying, FENG Bing, SU Zuqing, LU Chuanjian, ZHENG Guangjuan, TANG Lipeng

AIM: Psoriasis is a chronic inflammatory skin disease characterized by keratinocyte hyperproliferation and immune dysregulation, yet the spatial epigenetic and neuroimmune features within the skin remain poorly understood. This study aims to construct a spatial atlas of the neuroimmune and epigenetic microenvironment in psoriasis. METHODS: Formalin-fixed, paraffin-embedded skin tissue samples from five psoriasis patients and four healthy controls were stained with a 33-metal antibody panel targeting immune and epigenetic markers. Imaging data were processed to analyze immune cell composition, spatial relationships, and epigenetic marker distribution in psoriatic lesions. RESULTS: Analysis of over 163,000 cells from five psoriasis patients and four healthy controls revealed that psoriatic lesions have a more complex cellular composition than normal skin, including diverse immune subsets, endothelial cells, keratinocytes, and nerve fibers. Neighborhood analysis showed enrichment of multiple immune cells, such as CD14+ monocytes, CD4+/CD8+ T-lymphocytes (T cells), CD68+ macrophages, CD69+ tissue-resident memory T cells and CD20+ B-lymphocytes (B cells), and nerve fibers around keratinocytes. Notably, positive interactions were observed between cutaneous nerve fibers and specific immune cells (CD8+ T cells and CD68+ macrophages) as well as blood vessels. Additionally, histone H3 lysine 27 trimethylation (H3K27me3) modification was mapped across cell types and found in immune cells adjacent to keratinocytes. CONCLUSION: Imaging mass cytometry delineated the psoriatic microenvironment's multicellular structure integrating epigenetic and neuroimmune components, offering new insights into psoriasis pathogenesis.

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Original ResearchVol 42, Issue 6 • pp. 100-112DOI: 10.3969/j.issn.1000-4718.2026.06.009• Jan 15, 2026

Enterococcus faecalis Promotes Chemotherapy Resistance by Down-regulating MOB3B in Colorectal Cancer

Authors: ZHANG Weiyang, QI Jingru, ZHAO Zhuoyang, YANG Longan, YAN Yongrong, LI Yuxuan, SHUAI Xinran, WU Gongfa, SONG Jiawei, HUA Xing, ZHOU Rui, YU Lina

AIM: To investigate the contribution of Enterococcus faecalis (E. faecalis) to chemoresistance in colorectal cancer (CRC) and uncover the underlying mechanisms. METHODS: Bioinformatics analyses were performed to evaluate the expression of MOB3B, an Mps-one binder coactivator (MOB) protein family member, and its clinical implications in CRC patients. E. faecalis was co-cultured with CRC cells to assess its effect on MOB3B expression. MOB3B was overexpressed or silenced in CRC cells to determine its effects on cell viability and chemosensitivity. The LRRC19-dependent mechanism was investigated through additional bioinformatics analyses. Immunohistochemical staining of clinical CRC tissues was performed to correlate MOB3B expression with Tumour Regression Grade. RESULTS: MOB3B down-regulation was associated with adverse clinicopathological characteristics and poor prognosis in CRC patients. Co-culture with E. faecalis down-regulated MOB3B expression in CRC cells. MOB3B overexpression decreased cell viability, while its silencing increased viability. MOB3B overexpression also reversed chemoresistance in CRC cells. Bioinformatics analyses revealed that MOB3B modulated resistance to oxaliplatin and 5-fluorouracil in an LRRC19-dependent manner. Low MOB3B expression correlated with high Tumour Regression Grade in clinical tissues. CONCLUSION: These findings indicate that Enterococcus faecalis promotes chemotherapy resistance by down-regulating MOB3B in colorectal cancer, and that MOB3B may serve as a potential marker for evaluating chemosensitivity and prognosis in CRC patients. The role of E. faecalis abundance as a clinical biomarker requires further validation in prospective cohorts.

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Original ResearchVol 42, Issue 4 • pp. 100-112DOI: 10.3969/j.issn.1000-4718.2026.04.010• Jan 15, 2026

Calcium Sensitivity, but Not Its Level, Determines Hypoxic Constriction of Porcine Coronary Arteries

Authors: FAN Jinxia, WU Zhuozhi, NAN Yan, YAN Haochen, YAN Jiazhen, XIE Junjun, YING Lei, WANG Yang

AIM: Acute hypoxia can induce transient contraction of coronary arteries, leading to myocardial ischemia and even cardiac dysfunction. However, the precise regulatory mechanisms remain unclear. In this study, we applied various interventions to isolated porcine coronary arteries by modulating cytoplasmic calcium concentrations mediated by calcium channels on the plasma membrane and sarcoplasmic reticulum, aiming to investigate the relationship between hypoxic contraction and intracellular calcium levels as well as calcium sensitization effects. METHODS: Isolated rings of the porcine left anterior descending coronary artery served as the experimental model. Based on distinct intervention targets, four core experimental groups were established. The specific grouping, sample size (n) for each group, and treatments were as follows: (1) nitric oxide (NO)-soluble guanylyl cyclase (sGC) pathway and energy metabolism intervention groups including control (n=5), nitric oxide synthase inhibitor nitro-L-arginine (NLA, 10^-4 mol/L; n=4 to 5), soluble guanylyl cyclase (sGC) antagonist 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ, 3×10^-5 mol/L; n=5), endothelium-denuded (n=5), normal glucose incubation (n=3), and glucose-free incubation (n=3) groups; (2) calcium source intervention groups including normal calcium control (n=4), calcium-free incubation with 5×10^-3 mol/L ethylene glycol tetraacetic acid (EGTA; n=4), L-type calcium channel antagonist nifedipine (10^-6 mol/L; n=5 to 7), non-selective cation channel inhibitor NiCl2 (5×10^-5 mol/L; n=5 to 7), sarcoplasmic reticulum Ca²⁺-ATPase inhibitor thapsigargin (2×10^-6 mol/L; n=5 to 7), and inositol trisphosphate (IP3) receptor antagonist 2-aminoethoxydiphenyl borate (2-APB, 10^-4 mol/L; n=5 to 7) groups; (3) myosin light chain kinase (MLCK) pathway intervention groups including control (n=4) and MLCK-specific inhibitor 1-(5-iodonaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine hydrochloride (ML-7, 10^-5 mol/L; n=6) groups; (4) myosin light chain phosphatase (MLCP) activity and endothelium-dependence intervention groups including endothelium-intact (n=4) and mechanically endothelium-denuded (n=6) groups. All arterial rings were pre-contracted with either U46619 (3×10^-7 mol/L) or KCl (6×10^-2 mol/L) and then subjected to 10 minutes of hypoxia (95% N2+5% CO2). Changes in vascular tension were continuously monitored and recorded using a multi-channel physiological signal acquisition system. Furthermore, combined with Western blotting, the phosphorylation level of myosin light chain (MLC) and the activity of MLCP were determined; the phosphorylation levels of MLC and MLCP were also compared between endothelium-intact and endothelium-denuded coronary arteries under hypoxic conditions. RESULTS: (1) Hypoxic constriction of porcine coronary arteries is dependent on the activation of endothelium-derived nitric oxide (NO) and sGC in vascular smooth muscle cells. (2) Hypoxic contraction in porcine coronary arteries is independent of extracellular Ca²⁺ influx. (3) Hypoxic contraction in porcine coronary arteries does not rely on intracellular Ca²⁺ release from the sarcoplasmic reticulum. (4) Hypoxic contraction in porcine coronary arteries leads to inhibition of myosin light chain phosphatase activity, suggesting increased calcium sensitization in coronary artery smooth muscle. CONCLUSION: The mechanism underlying acute hypoxia-induced vasoconstriction exhibits distinct characteristics: it does not rely on extracellular calcium influx mediated by plasma membrane calcium channels, nor is it associated with intracellular calcium mobilization from sarcoplasmic reticulum stores. Instead, it is mediated by a significant enhancement in calcium sensitivity regulated by myosin light chain phosphatase, a process referred to as calcium sensitization.

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