Dataset Information

High expression of HOXB7 is an unfavorable prognostic factor for solid malignancies: A meta-analysis.

ABSTRACT:

Background

HOXB7 is abnormally expressed in a variety of tumors, but its prognostic value remains unclear due to sample size limitation and outcome inconsistency in previous studies. This meta-analysis was performed to explore the effect of HOXB7 expression on prognoses and clinicopathological factors in range of the whole solid tumors.

Methods

PubMed, EMBASE, and Web of Science databases were searched to identify included studies. Hazard ratios (HR) with its 95% confidence interval (CI) and clinicopathological factors were extracted. Subgroup analyses were performed according to histopathological type, tumor occurrence systems, and HOXB7 detection methods.

Results

A total of 3430 solid tumors patients from 20 studies (21 cohorts) were included in the meta-analysis. The results showed that high HOXB7 expression was significantly associated with worse survival (overall survival: HR = 1.98, 95%CI: 1.74-2.26, P < .001 and disease-free survival: HR = 1.59, 95%CI: 1.21-2.09, P = .001), more advanced tumor-node-metastasis (TNM) stage (odds ratio [OR] = 2.14, 95%CI: 1.68-2.73, P < .001), positive lymph node metastasis (OR = 2.16, 95%CI: 1.74-2.70, P < .001), more distant metastasis (OR = 1.63, 95%CI: 1.01-2.63, P = .048), poorer differentiation (OR = 1.48, 95%CI: 1.14-1.91, P = .003), and higher Ki-67 expression (OR = 2.53, 95%CI: 1.68-3.84, P < .001). Subgroup analysis showed that survival of patients with HOXB7 high expression was worse in either squamous cell carcinomas or non-squamous cell carcinomas, digestive tumors or non-digestive tumors, and protein level or mRNA level.

Conclusion

High HOXB7 expression might be a valuable biomarker of poor prognosis for solid tumors. HOXB7 promotes tumor proliferation and metastasis, and is associated with poorer differentiation, more advanced stage, even the chemotherapy resistance, suggesting that HOXB7 is a potential therapeutic target for solid tumors.

SUBMITTER: Zhou T

PROVIDER: S-EPMC8772762 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:Background: We obtained 2 types of clones which were termed SC (sphere-shaped clone) and NSC (non-sphere-shaped clone) from 4T1 cells by monoclonal culture. SC and NSC were distinct in morphology, surface marker, metabolism and proliferation rate. With the transcriptome sequencing data analysis, we found TMED2 expressed higher in SCs. TMED2 was a member of the transmembrane emp24 domain and might play roles in cancer cell proliferation. However, its prognostic roles in breast cancer remained unknown. We aimed to investigate the prognostic values of TMED2 in patients with breast cancer. Methods: We used UALCAN (http://ualcan.path.uab.edu) and the Human Protein Atlas (www.proteinatlas.org) to explore the TMED2 expression level and DNA methylation data between breast cancer and normal breast tissue. With Oncomine (www.oncomine.org), we investigated the copy number of TMED2 in breast cancer sample and normal breast tissue. We used the Kaplan-Meier Plotter database (http://kmplot.com/analysis) to analyze prognostic values of TMED2 mRNA expression in all breast cancers and in different intrinsic subtypes. Moreover, protein expression levels of TMED2 were confirmed by Western blot in breast cancer tissues and normal mammary tissue as well as SCs and NSCs. Results: TMED2 significantly upregulated in breast cancer patients compared to normal mammary samples. Meanwhile, the increased expression of TMED2 mRNA was closely associated with reduced overall survival (OS) in all breast cancers, and with reduced OS in patients with ER-positive, Luminal A or Luminal B breast cancer subtypes. Moreover, western blot confirmed that TMED2 increased expressed was correlated with the reduced OS at protein levels. Conclusion: Increased expression of TMED2 was significantly related to unfavorable outcomes in patients with breast cancer. Thus, we supposed TMED2 is oncogenic and a potential target for breast cancer therapy and these preliminary findings require further study to determine whether TMED2-targeting reagents might be developed for clinical application in breast cancer.