{"title":"Engineering vascular grafts from decellularized plants: Advances and challenges.","authors":"Nick Merna","doi":"10.14670/HH-18-934","DOIUrl":"10.14670/HH-18-934","url":null,"abstract":"<p><p>Small-caliber vascular grafts (<6 mm diameter) are critical for coronary and peripheral bypass surgeries, yet developing functional substitutes remains challenging. Autologous vessels are ideal but often unavailable or of poor quality. Synthetic grafts, such as expanded polytetrafluoroethylene (ePTFE) and Dacron, have high failure rates in small diameters due to thrombosis, intimal hyperplasia, and compliance mismatch. Tissue-engineered vascular grafts (TEVGs) aim to overcome these issues by providing a biocompatible scaffold with an endothelial lining. Decellularized plant tissues have recently gained attention as natural scaffolds for TEVGs due to their structural similarity to human vasculature. Leaves and stems provide an extracellular matrix (ECM) primarily composed of cellulose, which is biocompatible, porous, and non-thrombogenic. These scaffolds are cost-effective, scalable, and ethically uncontroversial. Decellularized parsley stems or leatherleaf leaves, for instance, can be recellularized with endothelial and smooth muscle cells (SMCs) to create small-diameter grafts that support endothelialization and withstand physiological pressures. Perfusion bioreactors further enhance the functionality of plant-based grafts by simulating physiological conditions. Pulsatile flow and pressure stimulate endothelial cell alignment, reducing thrombogenicity, while mechanical stimulation promotes SMC maturation and ECM deposition, improving graft strength and compliance. This review summarizes recent advances in plant-based vascular grafts and perfusion bioreactor conditioning, compares their performance to conventional grafts, and highlights remaining challenges. Decellularized plant scaffolds, with their inherent vascular architecture and biocompatibility, show promise as natural templates for small-caliber vascular grafts. However, further research is needed to address key challenges such as standardization, mechanical optimization, and long-term <i>in vivo</i> validation to facilitate their clinical application.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18934"},"PeriodicalIF":2.0,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142448","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ENO3 regulates ferroptosis by interaction with PKM2 to promote the progression of metabolic dysfunction-associated steatotic liver disease.","authors":"Zhenzi Cao, Xue Li, Qian Hao, Jing Liu, Minghao Li, Baoding Li, Shengjuan Hu, Yanling Li, Xiaofei Li, Yuanyuan Tang, Fuliang Pan, Yanxia Liu, Min Niu","doi":"10.14670/HH-18-933","DOIUrl":"https://doi.org/10.14670/HH-18-933","url":null,"abstract":"<p><strong>Background: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder characterized by excessive lipid accumulation in the liver. The glycolytic enzyme enolase 3 (ENO3) is reported to be most significantly elevated in the analysis of MASLD-related sequencing results based on the GEO database. However, the specific mechanism by which ENO3 regulates MASLD is not fully understood.</p><p><strong>Objective: </strong>To investigate the role and possible molecular mechanism of ENO3 in MASLD.</p><p><strong>Methods: </strong>The expression of ENO3 and PKM2 in the liver tissues of control and MASLD rats was detected by immunohistochemistry and western blot. <i>In vitro</i> studies involved treating THLE-2 cells with free fatty acids (FFA) and Ferrostatin-1 (Fer-1), as well as manipulating ENO3 expression via small interfering RNA (siRNA) and overexpression plasmids, and manipulating PKM2 expression via siRNA. Fat accumulation was assessed using Oil Red O staining and measurements of intracellular total cholesterol (TC) and triglycerides (TG). Ferroptosis markers, including SLC7A11, GPX4, Fe<sup>2+</sup>, and malondialdehyde (MDA), were evaluated. Protein-protein interactions between ENO3 and PKM2 were examined using co-immunoprecipitation (Co-IP) and immunofluorescence.</p><p><strong>Results: </strong>MASLD liver tissues exhibited significantly higher levels of ENO3 and PKM2. Silencing ENO3 in FFA-treated THLE-2 cells reduced fat accumulation, downregulated PKM2 expression, and decreased ferroptosis markers. Conversely, ENO3 overexpression promoted fat accumulation and ferroptosis, which were mitigated by Fer-1 or si-PKM2. Co-IP and immunofluorescence confirmed the physical interaction and co-localization of ENO3 and PKM2 in THLE-2 cells.</p><p><strong>Conclusions: </strong>ENO3 interacted with PKM2 to regulate ferroptosis and further promoted the progression of MASLD.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18933"},"PeriodicalIF":2.5,"publicationDate":"2025-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144119609","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Extracellular vesicles derived from different brain tissue cells: A potential therapeutic measure for hypoxic-ischemic brain injury in immature brains.","authors":"Yitong Guan, Lijun Yang, Hong Cui","doi":"10.14670/HH-18-932","DOIUrl":"https://doi.org/10.14670/HH-18-932","url":null,"abstract":"<p><p>Neonatal hypoxic-ischemic encephalopathy and neonatal acute ischemic stroke are common causes of hypoxic-ischemic brain injury (HIBI) in the neonatal period, which may lead to permanent neurological sequelae. It is difficult to distinguish the two in the early stage. As a timely brain protection measure, hypothermia is still the standard treatment, but its efficacy in the treatment of immature brain injury is still controversial. The underlying pathophysiological mechanisms and effective treatment strategies of neonatal hypoxic-ischemic brain damage (HIBD) have been an active area of research. Extracellular vesicles (EVs), a class of nanoscale membranous structures, play a critical role in intercellular communication by facilitating the transfer of bioactive molecules or engaging in receptor-mediated interactions. Recent studies have demonstrated that various cell types within brain tissue, including neurons, astrocytes, microglia, endothelial cells, and stem cells, secrete substantial amounts of EVs. These vesicles carry diverse cargo, such as microRNAs, DNA, and proteins, which exert regulatory effects on recipient cells within the brain, thereby mediating neuroprotective effects. These effects include enhancing synaptic plasticity, modulating neuroinflammation, promoting angiogenesis, and regulating cellular autophagy, collectively contributing to neuroprotection. This review aims to summarize the functional characteristics of EVs derived from different cell types within the brain and to highlight recent advancements in this field. By providing insights into the role of EVs in HIBI, it seeks to provide novel insights and references for understanding the pathogenesis of neonatal HIBI and exploring innovative therapeutic approaches.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18932"},"PeriodicalIF":2.5,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144110427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Pachymic acid ameliorates polycystic ovary syndrome via inactivating Akt/ERK signaling.","authors":"Dongmei Ji, Chunhua Zhang, Fang Fang, Yuanyuan Yi","doi":"10.14670/HH-18-931","DOIUrl":"10.14670/HH-18-931","url":null,"abstract":"<p><strong>Objective: </strong>Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder that adversely affects women's health and quality of life. Pachymic acid (PA), a bioactive ingredient from <i>Poria cocos</i> (Schw.) Wolf, has demonstrated protective effects against PCOS in a murine model. This study aims to investigate the underlying mechanism by which PA exerts protective effects against PCOS.</p><p><strong>Methods: </strong>Female Sprague-Dawley rats were treated with letrozole to induce PCOS. The ovarian granulosa cell line (KGN) was exposed to lipopolysaccharide (LPS) to mimic PCOS <i>in vitro</i>. Hematoxylin-eosin staining and TUNEL assay were used for ovarian histological analysis. The cell counting kit-8 assay was used to assess the viability of KGN cells. Flow cytometry was used for <i>in vitro</i> cell apoptosis analysis. Western blotting revealed molecular protein expression levels in rat ovaries and KGN cells.</p><p><strong>Results: </strong>PA attenuated LPS-induced lactate dehydrogenase release (p<0.01), reduced the cell apoptosis rate (p<0.001), Bax, and cleaved-caspase3 protein expression (p<0.001), and increased Bcl-2 protein expression (p<0.01) in KGN cells. PA attenuated letrozole-induced increases in testosterone (p<0.01), luteinizing hormone (p<0.01), and estradiol levels (p<0.05) and decreases in progesterone levels (p<0.05) in PCOS rats. PA promoted corpus luteum formation (p<0.001) and reduced the number of cystic follicles and cell apoptosis (p<0.001) in PCOS rats. PA blocked Akt and ERK signaling transduction in PCOS rats and KGN cells (p<0.001).</p><p><strong>Conclusion: </strong>PA protects against PCOS and attenuates cell apoptosis by inactivating Akt and ERK signaling.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18931"},"PeriodicalIF":2.5,"publicationDate":"2025-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077634","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Trophoblast-derived proteins and their effects on the pathogenesis of preeclampsia.","authors":"Ju Yang, Yanan Wang, Xueling Chen, Haifeng Zhang, Yunshan Xue, Haibin Chen","doi":"10.14670/HH-18-930","DOIUrl":"https://doi.org/10.14670/HH-18-930","url":null,"abstract":"<p><p>Trophoblast cells are crucial structural units of the placenta, responsible for maintaining its integrity and function. These cells synthesize and secrete specific proteins that play essential roles in placental vascularization, maternal and fetal immune tolerance, and other critical processes. An abnormal level of trophoblast-derived secreted proteins has been closely linked to pregnancy-related diseases. Preeclampsia, a severe complication of pregnancy characterized by <i>de-novo</i> development of hypertension and proteinuria after 20 weeks of gestation, poses significant health risks to both the mother and fetus. This article reviews several key trophoblast-derived proteins that are widely recognized for their roles in preeclampsia. The specific mechanisms of action and interconnections among these proteins in preeclampsia are discussed, along with novel insights into the underlying pathological mechanisms of this disease.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18930"},"PeriodicalIF":2.5,"publicationDate":"2025-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Periostin acts as an oncogene to promote laryngeal cancer progression by activating decorin.","authors":"Chao Wu, Bo Yang, Jiusheng Chu","doi":"10.14670/HH-18-804","DOIUrl":"10.14670/HH-18-804","url":null,"abstract":"<p><p>Laryngeal carcinoma (LC) is the second most common malignancy of the head and neck worldwide, with increasing incidence every year. However, the mechanism of its development is not completely clear. Periostin (POSTN) has been reported to be involved in various aspects of tumorigenesis. To determine the influence of POSTN on LC tumorigenesis, we first examined the expression of POSTN in tissues from patients with LC through immunohistochemistry, western blot, and qRT-PCR. Besides, we demonstrated that POSTN promoted LC cell migration, invasion, and proliferation <i>in vitro</i> by CCK-8, colony formation, and Transwell assays, and tumor growth <i>in vivo</i> by immunohistochemistry. Furthermore, the interaction between POSTN and decorin (DCN) was further verified by bioinformatics analysis and immunoprecipitation (IP), finding that POSTN promoted the malignant progression of LC by targeting DCN. Our findings support the idea that the level of POSTN expression and accumulation in tumors correlated with the malignancy degree of LC, suggesting that POSTN may play a potential role in improving laryngeal cancer treatment strategies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"687-696"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142345764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Tetsuichi Saito, Tomonori Minagawa, Naoki Yoshimura, Yi Luo, Yoshiyuki Akiyama
{"title":"Experimental murine models of interstitial cystitis/bladder pain syndrome: A review.","authors":"Tetsuichi Saito, Tomonori Minagawa, Naoki Yoshimura, Yi Luo, Yoshiyuki Akiyama","doi":"10.14670/HH-18-837","DOIUrl":"10.14670/HH-18-837","url":null,"abstract":"<p><p>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic enigmatic disease of the urinary bladder characterized by persistent bladder/pelvic pain in conjunction with lower urinary tract symptoms. IC/BPS is categorized as either Hunner-type IC (HIC) or BPS based on the presence/absence of the Hunner lesion, a reddish mucosal lesion in the bladder. HIC and BPS present with similar symptoms, however, the etiologies are completely different. Recent evidence suggests that HIC is an immune-mediated inflammatory disease of the urinary bladder. In contrast, BPS, other forms of HIC lacking Hunner lesions, is a minimally inflamed condition comprising various clinical phenotypes. Based on this evidence, basic research into IC/BPS has shifted to target each subtype of IC/BPS. Today, experimental murine models of autoimmune cystitis are used for HIC research, whereas models related to neurophysiological and psychosocial dysfunctions have been developed for BPS research. This emerging concept of a subtype-tailored approach may contribute to a better understanding of the full picture of IC/BPS, thereby improving current clinical management strategies and the development of novel therapies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"635-644"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Basel Elsayed, Amgad Mohamed Elshoeibi, Mohamed Elhadary, Abdullah M Al-Jubouri, Noof Al-Qahtani, Semir Vranic, Rafif Al-Saady
{"title":"Molecular and immunohistochemical markers in appendiceal mucinous neoplasms: A systematic review and comparative analysis with ovarian mucinous neoplasms and colorectal adenocarcinoma.","authors":"Basel Elsayed, Amgad Mohamed Elshoeibi, Mohamed Elhadary, Abdullah M Al-Jubouri, Noof Al-Qahtani, Semir Vranic, Rafif Al-Saady","doi":"10.14670/HH-18-830","DOIUrl":"10.14670/HH-18-830","url":null,"abstract":"<p><strong>Introduction: </strong>Appendiceal mucinous neoplasms (AMNs) represent a rare and diagnostically challenging group of tumors. This systematic review aims to summarize the reported molecular and immunohistochemical markers (IHC) associated with AMNs and compare them with ovarian mucinous neoplasms (OMNs) and colorectal adenocarcinoma (CRC).</p><p><strong>Methods: </strong>A comprehensive search was performed in PubMed/MEDLINE/PMC, Scopus, Embase, and Web of Science databases to identify studies looking at IHC and molecular markers in AMNs. Chi-squared and Fisher's exact tests were utilized to compare the marker expression across different tumor types.</p><p><strong>Results: </strong>We identified 27 articles reporting several potential biomarkers for distinguishing between different subtypes of AMNs. Mutations in <i>KRAS</i>, <i>GNAS</i>, and <i>RNF43</i> emerged as notable biomarkers, with <i>KRAS</i> mutations being the most prevalent across all subtypes. Additionally, p53 IHC overexpression was associated with higher tumor grades. When comparing AMNs with OMNs, we observed a higher prevalence of CK20, CDX2, SATB2, and MUC2 IHC expression, as well as <i>KRAS</i> and <i>GNAS</i> mutations, in AMNs. Conversely, CK7 and PAX8 IHC expression were more prevalent in OMNs. Comparing AMNs with CRCs, we found a higher prevalence of TOPO1 and PTEN IHC expression, as well as <i>KRAS</i> and <i>GNAS</i> mutations, in AMNs. Conversely, nuclear β-catenin IHC expression, as well as <i>TP53</i>, <i>APC</i>, and <i>PIK3CA</i> mutations, were more prevalent in CRCs.</p><p><strong>Conclusion: </strong>This systematic review identified possible markers for distinguishing AMNs and differentiating between AMNs, OMNs, or CRCs.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"621-633"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142914683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Does old-to-young kidney transplantation rejuvenate old donor kidneys?","authors":"Mayumi Takahashi-Kobayashi, Kunio Kawanishi, Joichi Usui, Satoshi Yamazaki, Surya V Seshan, Kunihiro Yamagata","doi":"10.14670/HH-18-829","DOIUrl":"10.14670/HH-18-829","url":null,"abstract":"<p><strong>Background: </strong>The number of older organ donors is increasing due to the aging population. Aged kidneys often face problems such as delayed graft function but previous murine experiments suggested the possibilities of rejuvenation, for example, in a parabiosis setting between old and young mice. To investigate kidney-graft rejuvenation, we compared an old-to-young (O-Y) patient transplantation group and a transplantation group with donors/recipients of approx. the same age (SA) with the renal senescence marker p16 in kidney biopsy samples at baseline and one year post-transplantation.</p><p><strong>Methods: </strong>We retrospectively analyzed our hospital's 32 cases of living-donor ABO-compatible transplants performed between 2013-2020. Both the baseline and one-year biopsy (n=9) or only the baseline biopsy (n=32) were analyzed. We divided the nine cases into an O-Y group (donors' median age 68 yrs, recipients 41, difference -27) and an SA group (donors' median age 53 yrs, recipients 51.5, difference -3.5). p16 was stained with the clones JC8 and E6H4 to determine the precise p16-positive rate.</p><p><strong>Results: </strong>The 32 baseline biopsies' p16-positive rate was weakly related to donor age, suggesting that the p16-positive rate can help evaluate kidney senescence. The (n=5) O-Y group's p16-positive rates were at baseline 0.08 and one year 0.12; the (n=4) SA group's rate was 0.03 at both baseline and one year.</p><p><strong>Conclusions: </strong>No kidney rejuvenation was observed, even when old donor kidneys went to young recipients.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"679-686"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"ABRACL upregulated by transcription factor CBX4 promotes proliferation and migration and inhibits the apoptosis of gastric cancer cells.","authors":"Kai Guo, Xiao Gao","doi":"10.14670/HH-18-812","DOIUrl":"10.14670/HH-18-812","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer (GC) is a predominant health concern in many countries. Actin-binding Rho activating C-terminal-like (ABRACL) belongs to a new family of low molecular weight proteins and has been implicated in cancers. This study was implemented to elucidate the role and mechanism of ABRACL in GC.</p><p><strong>Methods: </strong>The mRNA and protein expression of ABRACL and CBX4 in human gastric epithelium cell line GES-1 and GC cell lines was assessed with RT-qPCR and western blot. The transfection efficacy of sh-ABRACL, oe-CBX4, and sh-CBX4 was examined with RT-qPCR and western blot. AGS cell proliferation, migration, and invasion were evaluated using CCK-8, colony formation assay, wound healing, and Transwell assays, respectively. With western blot analysis, flow cytometry, and caspase-3 assay kits, the expressions of MMP2 and MMP9, cell apoptosis, and caspase-3 activity were estimated. Western blot was adopted to estimate the contents of apoptosis-related proteins. Luciferase reporter and chromatin immunoprecipitation (ChIP) were applied to verify the interaction between ABRACL and CBX4.</p><p><strong>Results: </strong>The expression of ABRACL and CBX4 was increased in GC tissues and cells. After interfering with ABRACL, the proliferation, migration, and invasion of GC cells were inhibited while apoptosis was promoted. We also discovered that CBX4 could bind to ABRACL and transcriptionally regulate ABRACL expression in AGS cells. Rescue experiments revealed that CBX4 overexpression partially reversed the regulatory effects of ABRACL silencing on the proliferation, migration, invasion, and apoptosis of GC cells.</p><p><strong>Conclusion: </strong>Collectively, ABRACL transcriptionally upregulated by CBX4 promoted the malignant progression of GC.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"721-732"},"PeriodicalIF":2.5,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}