A pan-cancer analysis of Wnt family member 7B in human cancers.

Background: Previous studies have highlighted the crucial role of Wnt7B in the development of various cancers, including breast, pancreatic, and gastric cancers. However, research into the involvement of Wnt7B is often confined to specific tumor types, with a noticeable lack of comprehensive studies spanning multiple cancer forms. The potential of Wnt7B as a diagnostic or prognostic cancer biomarker has not been fully explored. Methods: In this study, we combined bioinformatics and immunohistochemistry analyses to examine the expression patterns and functions of Wnt7B in cancerous and adjacent noncancerous tissues across a range of tumors. Results: Our data indicate that Wnt7B may serve as a novel prognostic biomarker and therapeutic target in certain cancers. Conclusion: We found significant upregulation of Wnt7B expression levels in the majority of cancer cases examined. Furthermore, Wnt7B can influence cancer prognosis by modulating the tumor microenvironment, immune cell infiltration, and tumor stemness, among other factors. Additionally, we examined the associations between anticancer drug sensitivity and Wnt7B expression, which could aid in the development of more precise clinical therapies.

Metal π-Lewis base activation in palladium(0)-catalyzed trans-alkylative cyclization of alkynals.

The Pd(0)-mediated umpolung reaction of an alkyne to achieve trans-difunctionalization is a potential synthetic methodology, but its insightful activation mechanism of Pd(0)-alkyne interaction has yet to be established. Here, a Pd(0)-π-Lewis base activation mode is proposed and investigated by combining theoretical and experimental studies. In this activation mode, the Pd(0) coordinates to the alkyne group and enhances its nucleophilicity through π-back-donation, facilitating the nucleophilic attack on the aldehyde to generate a trans-Pd(ii)-vinyl complex. Ligand-effect studies reveal that the more electron-donating one would accelerate the reaction, and the cyclization of the challenging flexible C- or O-tethered substrates has been realized. The origin of regioselectivities is also explicated by the newly proposed metal π-Lewis base activation mode.

Advances in Small-Molecule Dual Inhibitors Targeting EGFR and HER2 Receptors as Anti-Cancer Agents.

As members of the protein tyrosine kinase family, the Epidermal Growth Factor Receptor (EGFR) and Human Epidermal Growth Factor Receptor 2 (HER2) play essential roles in cellular signal transduction pathways. Overexpression or abnormal activation of EGFR and HER2 can lead to the development of various solid tumors. Therefore, they have been confirmed as biological targets for the development of anticancer drugs. Due to the fact that many cancers are highly susceptible to developing resistance to single-target EGFR inhibitors in clinical practice, dual inhibitors that target both EGFR and HER2 have been developed to increase efficacy, reduce drug resistance and interactions, and improve patient compliance. Currently, a variety of EGFR/HER2 dual inhibitors have been developed, with several drugs already approved for marketing or in clinical trials. In this review, we summarize recent advancements in small-molecule EGFR/HER2 dual inhibitors by focusing on structure-activity relationships and share novel insights into developing anticancer agents.

A brain-tumor neural circuit controls breast cancer progression in mice.

Tumor burden, considered a common chronic stressor, can cause widespread anxiety. Evidence suggests that cancer-induced anxiety can promote tumor progression, but the underlying neural mechanism remains unclear. Here, we used neuroscience and cancer tools to investigate how the brain contributes to tumor progression via nerve-tumor crosstalk in a mouse model of breast cancer. We show that tumor-bearing mice exhibited significant anxiety-like behaviors and that corticotropin-releasing hormone (CRH) neurons in the central medial amygdala (CeM) were activated. Moreover, we detected newly formed sympathetic nerves in tumors, which established a polysynaptic connection to the brain. Pharmacogenetic or optogenetic inhibition of CeMCRH neurons and the CeMCRH→lateral paragigantocellular nucleus (LPGi) circuit significantly alleviated anxiety-like behaviors and slowed tumor growth. Conversely, artificial activation of CeMCRH neurons and the CeMCRH→LPGi circuit increased anxiety and tumor growth. Importantly, we found alprazolam, an antianxiety drug, to be a promising agent for slowing tumor progression. Furthermore, we show that manipulation of the CeMCRH→LPGi circuit directly regulated the activity of the intratumoral sympathetic nerves and peripheral nerve-derived norepinephrine, which affected tumor progression by modulating antitumor immunity. Together, these findings reveal a brain-tumor neural circuit that contributes to breast cancer progression and provide therapeutic insights for breast cancer.

A first-in-class HBO1 inhibitor WM-3835 inhibits castration-resistant prostate cancer cell growth in vitro and in vivo.

The prognosis and overall survival of castration-resistant prostate cancer (CRPC) patients are poor. The search for novel and efficient anti-CRPC agents is therefore extremely important. WM-3835 is a cell-permeable, potent and first-in-class HBO1 (KAT7 or MYST2) inhibitor. Here in primary human prostate cancer cells-derived from CRPC patients, WM-3835 potently inhibited cell viability, proliferation, cell cycle progression and in vitro cell migration. The HBO1 inhibitor provoked apoptosis in the prostate cancer cells. It failed to induce significant cytotoxicity and apoptosis in primary human prostate epithelial cells. shRNA-induced silencing of HBO1 resulted in robust anti-prostate cancer cell activity as well, and adding WM-3835 failed to induce further cytotoxicity in the primary prostate cancer cells. Conversely, ectopic overexpression of HBO1 further augmented primary prostate cancer cell proliferation and migration. WM-3835 inhibited H3-H4 acetylation and downregulated several pro-cancerous genes (CCR2, MYLK, VEGFR2, and OCIAD2) in primary CRPC cells. Importantly, HBO1 mRNA and protein levels are significantly elevated in CRPC tissues and cells. In vivo, daily intraperitoneal injection of WM-3835 potently inhibited pPC-1 xenograft growth in nude mice, and no apparent toxicities detected. Moreover, intratumoral injection of HBO1 shRNA adeno-associated virus (AAV) suppressed the growth of primary prostate cancer xenografts in nude mice. H3-H4 histone acetylation and HBO1-dependent genes (CCR2, MYLK, VEGFR2, and OCIAD2) were remarkably decreased in WM-3835-treated or HBO1-silenced xenograft tissues. Together, targeting HBO1 by WM-3835 robustly inhibits CRPC cell growth.

Immune-related ureteritis and cystitis induced by immune checkpoint inhibitors: Case report and literature review.

Immune checkpoint inhibitors (ICIs), including anti-cytotoxic T lymphocyte-associated protein 4 (anti-CTLA4) and anti-programmed death cell protein 1 (anti-PD-1), are increasingly prescribed in metastatic carcinoma therapy. ICI-related kidney injury is gradually recognized by clinicians. However, immune-related ureteritis and cystitis easily go undiagnosed. We report three cases of PD-1 monoclonal antibody (mAb)-related ureteritis and cystitis. We further carried out a review of the literature about ICI-related ureteritis and cystitis. The cases in our reports manifest urinary irritation, sterile pyuria, gross hematuria, hydronephrosis, dilation of the ureters, and acute kidney injury. Urinary irritation improved effectively; urinalysis and renal function returned to normal after glucocorticoid therapy. During ICI therapy, urinalysis and renal function and urinary imaging examination are recommended to be monitored regularly. It contributes to identify immune-related ureteritis/cystitis earlier to efficiently alleviate urinary symptoms and immunologic urinary tract injury through glucocorticoid therapy while avoiding the abuse of antibiotics.

A Review of Recent Advances in Nanomaterial-based Stem Cell Therapy and the Corresponding Risks.

Stem cell therapy is widely regarded as a promising strategy in regenerative medicine, yet the therapeutic effects of stem cells in vivo are limited by many factors when applied without additional factors, such as poor cell engraftment, uncontrolled differentiation, and unclear cell fates and niches. The emergence of nanotechnology has provided several solutions for these problems. Nanomaterial-based cell labeling and tracking have been extensively investigated in recent decades, and many innovative and multifunctional nanomaterials have been used to reveal the fate of stem cells, allowing more efficient, sensitive, and accurate imaging/tracking strategies for stem cells to be achieved. Nanomaterials enhance stem cell therapy by incorporating or integrating with stem cells and, as scaffolds or substrates, nanomaterials with antioxidant properties that can be used as graft coatings show great promise for clinical transformation. However, current reviews on the subject tend to focus on the various effects of nanomaterials on stem cells and are less concerned with their application to stem cell therapy. Accordingly, we herein present a review of progress in the application of nanomaterials in stem cell therapy over the last three years, which we hope will be of benefit to a comprehensive understanding of nanomaterial-mediated stem cell therapy from lab to pre-clinical practice.

Mechanochromic luminescence properties of fluoro-substituted pinene-containing cyclometalated platinum(II) complexes with multiple triplet excited states.

The structure-mechanochromism relationship is explored with respect to packing patterns and corresponding intermolecular interactions that are affected by the number and location of -F. The distinct and reversible mechanochormic luminescence (Δλem up to ca. 90 nm) of yellow solids (-)-1-Yg, (-)-2-Yg, and (-)-3-Yg was displayed with a simultaneous crystal-to-amorphous transformation. The change of multiple triplet excited states accounted for the mechanochormic luminescence, and a switch from the 3π,π* monomer to the excimer/3MMLCT occurred in the grinding process. The mechanical force led to perturbation in the molecular packing, and aggregates with effective PtPt and π-π interactions were formed in the amorphous phase, leading to the variation of excited states. The mechanochromic luminescence could be reverted by dropping in CH2Cl2 and could be cycled multiple times without perceivable performance degradation. This work gives a reference for designing mechanochromic luminescent materials toward multicolor and multicomponent responses.

The emerging roles of dual-specificity phosphatases and their specific characteristics in human cancer.

Reversible phosphorylation of proteins, controlled by kinases and phosphatases, is involved in various cellular processes. Dual-specificity phosphatases (DUSPs) can dephosphorylate phosphorylated serine, threonine and tyrosine residues. This family consists of 61 members, 44 of which have been identified in human, and these 44 members are classified into six subgroups, the phosphatase and tensin homolog (PTEN) protein phosphatases (PTENs), mitogen-activated protein kinase phosphatases (MKPs), atypical DUSPs, cell division cycle 14 (CDC14) phosphatases (CDC14s), slingshot protein phosphatases (SSHs), and phosphatases of the regenerating liver (PRLs). Growing evidence has revealed dysregulation of DUSPs as one of the common phenomenons and highlighted their key roles in human cancers. Furthermore, their differential expression may be a potential biomarker for tumor prognosis. Despite this, there are still many unstudied members of DUSPs need to further explore their precise roles and mechanism in cancers. Most importantly, the systematic review is very limited on the functional/mechanistic characteristics and clinical application of DUSPs at present. In this review, the structures, functions and underlying mechanisms of DUSPs are systematically reviewed, and the molecular and functional characteristics of DUSPs in different tumor types according to the current researches are summarized. In addition, the potential roles of the unstudied members and the possible different mechanisms of DUSPs in cancer are discussed and classified based on homology alignment and structural domain analyses. Moreover, the specific characteristics of their expression and prognosis are further determined in more than 30 types of human cancers by using the online databases. Finally, their potential application in precise diagnosis, prognosis and treatment of different types of cancers, and the main possible problems for the clinical application at present are prospected.

Homeobox-A13 acts as a functional prognostic and diagnostic biomarker via regulating P53 and Wnt signaling pathways in lung cancer.

BACKGROUND: The prognosis of lung cancer patients is poor without useful prognostic and diagnostic biomarker. To search for novel prognostic and diagnostic markers, we previously found homeobox-A13 (HOXA13) as a promising candidate in lung cancer. OBJECTIVE: To determine the precisely clinical feature, prognostic and diagnostic value, possible role and mechanism of HOXA13. METHODS: Gene-expression was explored by real-time quantitative-PCR, western-blot and tissue-microarray. The associations were analyzed by Chi-square test, Kaplan-Meier and Cox-regression. The roles and mechanisms were evaluated by MTS, EdU, transwell, xenograft tumor and luciferase-reporter assays. RESULTS: HOXA13 expression is increased in tumors, and correlated with age of patients. HOXA13 expression is associated with unfavorable overall survival and relapse-free survival of patients in four cohorts. Interestingly, HOXA13 has different prognostic significance in adenocarcinoma (ADC) and squamous-cell carcinoma (SCC), and is a sex- and smoke-related prognostic factor only in ADC. Importantly, HOXA13 can serve as a diagnostic biomarker for lung cancer, especially for SCC. HOXA13 can promote cancer-cell proliferation, migration and invasion in vitro, and facilitate tumorigenicity and tumor metastasis in vivo. HOXA13 acts the oncogenic roles on tumor growth and metastasis by regulating P53 and Wnt/ß-catenin signaling activities in lung cancer. CONCLUSIONS: HOXA13 is a new prognostic and diagnostic biomarker associated with P53 and Wnt/ß-catenin signaling pathways.

Pulmonary benign metastasizing leiomyoma: a case report and literature review.

Benign metastasizing leiomyoma (BML) is a rare condition that occurs mainly in premenopausal women and is characterized most commonly by pulmonary metastases. Here, we report the case of a 45-year-old woman who presented with multiple bilateral pulmonary nodules on chest examination during a health checkup 13 years after myomectomy. This patient has a normal menstrual cycle, moderate anemia, and no obvious respiratory symptoms. Serum concentrations of cancer markers such as carcinoembryonic antigen, neuron specific enolase, cytokeratin 19 fragments, and pro-gastrin-releasing peptide were within normal limits. Color doppler ultrasound was also performed, several hypoechoic regions were found in uterine bodies and cavity. The computed tomography (CT)-guided lung biopsy was used for histopathological examination. Immunohistochemical staining revealed BML which were positive for smooth muscle antibody, desmin, vimentin, estrogen and progesterone receptors, and Ki-67 positive rate of about 1%. Hysterectomy and bilateral adnexectomy were performed as a part of treatment. The lung nodules were meticulously monitored at follow-up. Three months later, the repeat CT scan showed that the nodules had reduced in size, and no new nodules had appeared, 1 year later, CT scan showed no obvious changes in lung nodules. This study is of great significance as the results will be helpful in diagnosing and treating future pulmonary benign metastasizing leiomyoma (PBML) cases.

Icaritin enhances the efficacy of cetuximab against triple-negative breast cancer cells.

Triple-negative breast cancer (TNBC) has a greater risk of recurrence and metastasis along with a worse prognosis compared with other subtypes of breast cancer. Studies have revealed that mitogenic estrogen signaling is involved in the malignant proliferation of TNBC cells through a novel variant of the estrogen receptor, estrogen receptor α-36 (ER-α36). The results of the present study demonstrated that knockdown of ER-α36 expression in TNBC cells using short hairpin RNA inhibited rapid estrogen signaling bypass activation of the PI3K/AKT signaling pathway. Moreover, the ER-α36 modulator icaritin inhibited the proliferation of TNBC cells both in vitro and in vivo. Here, it was revealed that the combination of icaritin and cetuximab, a therapeutic epidermal growth factor receptor (EGFR) neutralizing antibody, induced apoptosis and inhibited cell proliferation synergistically in TNBC cells. The results of the present study improved the understanding of the underlying mechanisms of TNBC progression and supported the therapeutic potential of combined treatment targeting the ER-α36 and EGFR.

The role of WT1 in breast cancer: clinical implications, biological effects and molecular mechanism.

Although Wilms' tumor gene 1 (WT1) was first cloned and identified as a tumor suppressor gene in nephroblastoma, subsequent studies have demonstrated that it can also play an oncogenic role in leukemia and various solid tumors. WT1 exerts biological functions with high tissue- and cell-specificity. This article reviews the relationship between WT1 and breast cancer from two aspects: (1) clinical application of WT1, including the relationship between expression of WT1 and prognosis of breast cancer patients, and its effectiveness as a target for comprehensive therapy of breast cancer; (2) the biological effects and molecular mechanisms of WT1 in the development and progression of breast cancer, including proliferation, apoptosis, invasion, and metastasis of breast cancer cells.

Long Non-coding Wilms Tumor 1 Antisense RNA in the Development and Progression of Malignant Tumors.

A growing number of studies have shown that long non-coding RNAs (lncRNAs) play an important role in tumor development and progression and are key molecules affecting tumor progression. The lncRNA Wilms tumor 1 antisense RNA (WT1-AS) is specifically expressed in various malignant tumors. In particular, WT1-AS expression is upregulated in colon cancer and breast cancer but is significantly downregulated in cervical cancer, liver cancer, and kidney cancer. The level of WT1-AS expression is closely related to the size, stage, and patient survival rate of these cancers. In this article, we review the modes of action, expression, function, and mechanisms of WT1-AS in different tumors to provide new targets for tumor diagnosis and treatment.

CD5+MYC+ predicts worse prognosis in diffuse large B-cell lymphoma.

The dual expression of CD5 and MYC protein (DECM) on B-lymphocytes may arise at a specific stage of de novo diffuse large B-cell lymphoma (DLBCL). This study retrospectively reviewed 210 patients with de novo DLBCL at the Affiliated Hospital of Jiangnan University between 2006 and 2017. DECM was significantly correlated with a worse prognosis than that in either the CD5+ or MYC+ or CD5-MYC- patients. Furthermore, patients with DECM showed a similar outcome to MYC+BCL2+ lymphoma patients who have extremely poor survival rates. Multivariate analysis demonstrated that DECM was a significant independent predictor for overall survival (P < .0001) and progression-free survival (P < .0001) in DLBCL. DLBCL patients with DECM showed significantly inferior clinical outcomes compared to the CD5+, MYC+ or CD5-MYC- patients. Combinational therapeutic modalities might be a candidate approach to improve the prognosis of these patients.

Multifaceted regulation and functions of fatty acid desaturase 2 in human cancers.

As an important hallmark of metabolic reprogramming in cancer, a disruption in fatty acid metabolism contributes to tumor proliferation, cell migration and invasion, and other tumor cell behaviors. In recent years, more and more studies have been conducted on fatty acid desaturase 2 (FADS2), the first rate-limiting enzyme for the biosynthesis of polyunsaturated fatty acids. These studies have found that FADS2 is abnormally expressed in cancers of the breast, lung, liver, and esophagus; melanoma; leukemia; and other malignant tumors. Furthermore, its expression is significantly correlated with tumor proliferation, cell migration and invasion, clonal formation, angiogenesis, ferroptosis, resistance to radiotherapy, histological grade, metastasis to lymph nodes, clinical stage, and prognosis. The abnormal expression of FADS2 results in an imbalance of cell membrane phospholipids, which disrupts the fluidity of the membrane structure and the transmission of signals and promotes the production of proinflammatory factors and arachidonic acid (AA) metabolites, ultimately harming human health. This article aims to systematically review the structural characteristics of FADS2; its function, expression, and mechanism of action; and the factors affecting its activity. This review also provides new ideas and strategies for the development of treatments aimed at the metabolic reprogramming of tumors.

Mechanism, safety and efficacy of three tyrosine kinase inhibitors lapatinib, neratinib and pyrotinib in HER2-positive breast cancer.

The incidence of breast cancer ranks first among female malignant tumors that affect women's health. Epidermal growth factor receptor (EGFR) family overexpression, especially human epidermal receptor2 (HER2), features prominently in breast cancer with a significant relation to poor prognosis. Currently, specific monoclonal antibodies and tyrosine kinase inhibitors (TKIs) are the two HER2 targeting strategies that have successfully improved the prognosis of patients with HER2-positive breast cancer. This paper focuses on three officially approved TKIs for HER2 breast cancer, namely, lapatinib, neratinib and pyrotinib, and systematically reviews the mechanism, safety, efficacy and resistance of these TKIs.

Up-regulated Wnt1-inducible signaling pathway protein 1 correlates with poor prognosis and drug resistance by reducing DNA repair in gastric cancer.

BACKGROUND: Wnt1-inducible signaling pathway protein 1 (WISP1) is upregulated in several types of human cancer, and has been implicated in cancer progression. However, its clinical implications in gastric cancer (GC) remain unclear. AIM: To explore the expression pattern and clinical significance of WISP1 in GC. METHODS: Public data portals, including Oncomine, The Cancer Genome Atlas database, Coexpedia, and Kaplan-Meier plotter, were analyzed for the expression and clinical significance of WISP1 mRNA levels in GC. One hundred and fifty patients who underwent surgery for GC between February 2010 and October 2012 at the Affiliated Hospital of Jiangnan University were selected for validation study. WISP1 levels were measured at both the mRNA and protein levels by RT-qPCR, Western blot analysis, and immunohistochemistry (IHC). In addition, the in situ expression of WISP1 in the GC tissues was determined by IHC, and the patients were accordingly classified into high- and low-expression groups. The correlation of WISP1 expression status with patient prognosis was then determined by univariate and multivariate Cox regression analyses. WISP1 was knocked down by RNA interference. The 50% inhibitory concentration of oxaliplatin was detected by CellTiter-Blue assay. RESULTS: WISP1 levels at both the mRNA and protein levels were remarkably upregulated in GC tissues compared to normal tissues. Moreover, IHC revealed that WISP1 expression was associated with T stage and chemotherapy outcome, but not with lymph node metastasis, age, gender, histological grade, or histological type. GC patients with high WISP1 expression showed a poor overall survival. Multivariate survival analysis indicated that WISP1 was an important prognostic factor for GC patients. Mechanistically, knock-down of WISP1 expression enhanced sensitivity to oxaliplatin by reducing DNA repair and enhancing DNA damage. CONCLUSION: Significantly upregulated WISP1 expression is associated with cancer progression, chemotherapy outcome, and prognosis in GC. Mechanistically, knock-down of WISP1 expression enhances oxaliplatin sensitivity by reducing DNA repair and enhancing DNA damage. WISP1 may be a potential therapeutic target for GC treatment or a potential biomarker for diagnosis and prognosis.

Vestigial like family member 3 is a novel prognostic biomarker for gastric cancer.

BACKGROUND: Vestigial like family member 3 (VGLL3) is associated with the prognosis of epithelial ovarian cancer and soft tissue sarcoma, but its role in gastric cancer (GC) is unclear. AIM: To explore the expression pattern and clinical significance of VGLL3 in GC. METHODS: Integrative analysis was performed on the GC transcriptome profiles and survival information deposited in the ONCOMINE, GEPIA, and ONCOLNC databases. The expression levels of VGLL3 mRNA and protein were analyzed in the freshly resected tumor and normal gastric tissues from GC patients by quantitative RT-PCR and Western blot, respectively. In addition, the in situ expression of VGLL3 in the GC tissues was determined by immunohistochemistry (IHC), and the patients were accordingly classified into the high and low expression groups. The correlation of VGLL3 expression status with patient prognosis was then determined by univariate and multivariate Cox regression analyses. RESULTS: Analysis of the ONCOMINE and GEPIA databases showed that VGLL3 was significantly up-regulated in GC tissues (P = 0.003), and associated with the tumor TNM stage (P = 0.0163). The high VGLL3 expression group had a significantly worse prognosis compared to the low expression group, as per both GEPIA (P = 0.0057) and ONCOLNC (P = 0.01). The bioinformatics results were validated by the significantly higher VGLL3 mRNA and protein levels in the GC tissues compared to the adjacent normal tissues (P < 0.001) in a cohort of 30 GC patients. Furthermore, high in situ expression of VGLL3 protein was associated with more advanced N and TNM stages and HER2 mutation (P < 0.05) in a cohort of 172 patients. Kaplan-Meier analysis showed that the high VGLL3 expression group had a worse prognosis compared to the low expression group (P = 0.019). Multivariate analysis showed that VGLL3 expression status was an independent risk factor for prognosis. In addition, the prognostic risk model nomogram showed that VGLL3 was the most important indicator, with an area under the receiver operating characteristic (ROC) curve (AUC) of 0.613 for 3-year survival and 0.706 for 5-year survival. Finally, the protein interaction network analysis revealed that VGLL3 is likely involved in the Hippo signaling pathway. CONCLUSION: VGLL3 is overexpressed in GC tissues and associated with a poor prognosis, indicating its potential as a novel prognosis biomarker and therapeutic target for GC.

Clinical correlation of B7-H3 and B3GALT4 with the prognosis of colorectal cancer.

AIM: To investigate the expression and clinical significance of B7 homolog 3 (B7-H3) and ß-1,3-galactosyltransferase-4 (B3GALT4) in colorectal cancer (CRC) patients. METHODS: Using tissue microarray, we identified the expression of B7-H3 and B3GALT4 in 223 CRC patient samples by immunohistochemistry and evaluated the possible correlation between B7-H3 and B3GALT4 and clinical outcomes. Further, the mRNA and protein expression were identified to establish the regulatory relationship of B7-H3 with B3GALT4 in vitro. RESULTS: A significant positive correlation between B7-H3 and B3GALT4 was observed in CRC specimens (r = 0.219, P = 0.001). High expression of B7-H3 was identified as a significant independent predictor of poor overall survival (OS) [hazard ratio (HR) = 1.781; 95%CI: 1.027-3.089; P = 0.040]. Moreover, high expression of B3GALT4 was also recognized as an independent predictor of inferior OS (HR = 1.597; 95%CI: 1.007-2.533; P = 0.047). Additionally, CRC patients expressing both high B7-H3 and high B3GALT4 contributed to a significant decrease in OS (HR = 2.283; 95%CI: 1.289-4.042; P = 0.005). In CRC cell lines with stable expression of high B7-H3, the mRNA and protein expressions of B3GALT4 were significantly upregulated. Similarly, the expression of B3GALT4 was significantly reduced when expression of B7-H3 was knocked down. CONCLUSION: The expression of B3GALT4 in CRC is positively correlated with B7-H3 expression in vitro. B7-H3/B3GLAT4 may be used as dual prognostic biomarkers for CRC.