Histology and histopathology, Vol.41, Nº1, (2026)

Ir a Estadísticas

Permanent URI for this collection

http://hdl.handle.net/10201/180689

Browse

Recent Submissions

Now showing 1 - 5 of 15
  • Thumbnail Image
    Item
    Open Access
    AHSA1 promotes the progression of lung cancer by enhancing the expression of HSP90α
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Zifeng Jiang; Kun Gao; Min Wang; Biología Celular e Histología
    Background. Lung cancer (LC) is a leading cause of malignancy-related morbidity and mortality worldwide. The activator of 90 kDa heat shock protein ATPase homolog 1 (AHSA1), one of the chaperones of heat shock protein 90 kDa (heat shock protein 90, HSP90), is involved in the maturation, stabilization, degradation, and function of oncogenic proteins. The aim of this study was to investigate the specific mechanism and role of AHSA1 in LC development. Methods. Expression of AHSA1 in LC was analyzed using The Cancer Genome Atlas (TCGA) database. AHSA1 expression in LC cells and tissues was assessed by qRT-PCR and western blotting. In addition, Kaplan-Meier plotter analysis and univariate and multivariate Cox analyses were used to evaluate the relationship between AHSA1 and clinicopathological variables and prognosis. The effects of AHSA1 on LC cell proliferation and migration were observed using cell counting kit-8, flow cytometry, wound healing, and Transwell assays. Target genes were predicted by bioinformatics and subsequently validated using a qRT-PCR assay. Results. AHSA1 exhibited significant upregulation in LC tissues and cell lines, with its elevated expression correlating with adverse prognostic outcomes in LC patients. Functional assays revealed that downregulation of AHSA1 markedly impedes the proliferation, migration, and invasion of LC cells. Conversely, overexpression of AHSA1 enhanced these malignant behaviors. Furthermore, bioinformatics analysis suggested a potential interaction between AHSA1 and HSP90α, which was also found to be highly expressed in LC cells, exhibiting a notable increase in expression levels following AHSA1 upregulation. Conclusions. AHSA1 is implicated in promoting the progression of LC by enhancing the malignant phenotype of cancer cells through the upregulation of HSP90α expression, which may underlie the association of AHSA1 expression with adverse clinicopathologic features in LC patients. These findings indicate that AHSA1 serves as a potential prognostic biomarker and represents a viable therapeutic target for LC
  • Thumbnail Image
    Item
    Open Access
    HMMR inhibition by 4-methylumbelliferone is effective in preclinical hepatocellular carcinoma models
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Ge Sang Wang Dui2; Suo Lang Bai Ma; Ci Yang; Wen Xu; Jianguo Xu; Ying Zhu; Biología Celular e Histología
    The poor prognosis of hepatocellular carcinoma (HCC), especially in advanced stages, underscores the need for new therapeutic strategies. In this study, we show that hyaluronan-mediated motility receptor (HMMR) is highly expressed in HCC tumors compared with normal liver tissues. Knockdown of HMMR using siRNA significantly reduced cell proliferation and migration in both parental and doxorubicin-resistant HCC cell lines without inducing apoptosis. Similarly, treatment with 4-Methyl-umbelliferone (4-MU), a pharmacological HMMR inhibitor, led to dose-dependent decreases in proliferation and migration in vitro. In vivo, 4-MU treatment significantly inhibited tumor growth in a HepG2 xenograft model, resulting in a 44% reduction in tumor volume by day 20 and an 80% decrease in HMMR expression in tumor tissues. These results demonstrate that HMMR promotes growth and migration in HCC, and targeting HMMR effectively inhibits both parental and drug-resistant HCC cells. Additionally, our findings suggest that 4-MU, an approved drug for biliary tract disorders, holds promise as a repurposed therapeutic candidate for HCC treatment.
  • Thumbnail Image
    Item
    Open Access
    Tuoli Xiaodu powder ameliorated 5-fluorouracil-induced intestinal injury by reducing intestinal inflammation, oxidative stress, and intestinal flora imbalance
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Ling Jiang; Wanrou Jiang; Wanyi Zhang; Wenjuan Zheng; Hongjie Huang; Yu Xia; Xiuyun He; Chaofu Zhu; Yongjun Wu; Biología Celular e Histología
    Chemotherapy-induced diarrhea (CID) is a common adverse event in cancer patients treated with 5-fluorouracil (5-FU). This study aimed to investigate the potential protective effects of Tuoli Xiaodu (TLXD) powder on CID and to explore its possible mechanisms. Mice with CID induced by 5-FU were randomly divided into seven groups: Blank group, CID group, positive drug (loperamide) group, and TLXD powder low, medium, and high groups. The degree of diarrhea, tumor growth, intestinal barrier damage, intestinal inflammation, oxidative stress, and gut microbiota diversity were assessed. The study showed that TLXD powder significantly inhibited diarrhea and tumor growth in 5-FU-induced CID mice. H&E staining and western blot showed that TLXD powder improved the intestinal mucosa and intestinal permeability of 5-FU-induced CID mice. Furthermore, TLXD powder elicited a reduction in the expression of inflammatory factors within the intestinal tract of mice with CID while simultaneously augmenting the expression of anti-inflammatory factors and maintaining a balanced Th17/Treg ratio. TLXD powder decreased intestinal oxidative stress and intestinal epithelial cell ferroptosis and activated the Nrf2/HO-1 signaling axis in CID mice. The results of the gut flora analysis showed that TLXD powder improved the intestinal flora structure of CID mice. TLXD powder significantly reduced the proportion of Proteobacteria, Actinobacteria, Deferribacteres, and TM7 at the phylum level and Desulfovibrio, Mucispirillum, Adlercreutzia, and Odoribacter at the genus level. These findings provide a new therapeutic approach for the management of CID in cancer patients treated with 5-FU
  • Thumbnail Image
    Item
    Open Access
    Therapeutic potential of porphyran in mitigating ischemia-reperfusion injury in gerbil hippocampus
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Tae-Kyeong Lee; Joon Ha Park; Dae Won Kim; Choong-Hyun Lee; Moo-Ho Won; Il Jun Kang; Ji Hyeon Ahn; Biología Celular e Histología
    Cerebral ischemia-reperfusion (IR) injury is a critical pathological event that leads to extensive neuronal loss, neuroinflammation, and blood-brain barrier (BBB) dysfunction. Porphyran, a sulfated polysaccharide derived from Porphyra spp., has demonstrated anti-inflammatory and neuroprotective effects in various neurological conditions. This study aimed to evaluate the post-ischemic therapeutic potential of porphyran in a gerbil model of transient forebrain ischemia. Our findings reveal that porphyran administration (50 mg/kg orally once daily for five days) following IR significantly mitigated IR-induced cognitive decline, as evidenced by the Y-maze test, but porphyran treatment did not significantly prevent neuronal death in the CA1 subregion of the hippocampus, as revealed by Cresyl Violet (CV) and Fluoro-Jade B (FJB) staining. However, porphyran treatment after IR injury effectively attenuated the IR-induced decrease in acetylcholine (ACh) levels, suggesting potential preservation of cognitive function in surviving neurons. Furthermore, porphyran significantly mitigated microglial activation and reduced the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), indicating its anti-inflammatory properties. Additionally, porphyran administration reduced BBB disruption, as evidenced by decreased extravasation of immuno-globulin G (IgG), suggesting a role in maintaining vascular integrity. In summary, although porphyrin administration after IR does not protect pyramidal neurons directly, it may improve cognitive function by mitigating ACh depletion, suppressing microglial activation, and reducing inflammatory cytokine levels
  • Thumbnail Image
    Item
    Open Access
    KIF22 promotes the proliferation and immune escape of endometrial cancer cells by activating the STAT3/PDL1 pathway
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Chaohe Zhang; Chaoqun Wang; Biología Celular e Histología
    Objective. Endometrial cancer (EC) is a common gynecologic malignancy with high morbidity and mortality. Kinesin Family member 22 (KIF22) is regarded as a critical oncogene, but its functions in EC progression remained elusive. Hence, this research elucidated the role of KIF22 in EC development and studied the possible mechanism. Methods. KIF22 expression in EC and the relationship with the overall survival of EC cases were determined by GEPIA and online K-M plotter. After transfection with sh-KIF22, cell viability and invasion were evaluated utilizing CCK-8 and Transwell assays. The content of IFN-γ, IL-2, and TNF-α was assessed utilizing an ELISA assay. The protein levels of p-STAT3, STAT3, and PD-L1 were examined using western blot. A xenograft tumor was constructed to assess tumor growth. Results. KIF22 was elevated in EC, with high KIF22 levels presenting poor overall survival. Additionally, silenced KIF22 restrained EC cell viability, invasion ability, and STAT3/PD-L1 pathway, enhanced the viability of CD8+ T cells, and elevated the levels of IFN-γ, IL-2, and TNF-α. Moreover, the rescue assay revealed that STAT3 overexpression counteracted the inhibitory effect of silenced KIF22 on EC cell proliferation, invasion and immune escape. Furthermore, silenced KIF22 repressed EC tumor growth and p-STAT3 and PD-L1 levels, and elevated the IFN-γ level in vivo. Conclusion. The findings demonstrated that KIF22 was elevated in EC and correlated with a poor prognosis. Silenced KIF22 repressed cell proliferation, invasion, and immune escape via suppressing the STAT3/PD-L1 pathway in EC.