Heng Zhou
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Heng Zhou has a total of 38 co-authors. Here are the top co-authors by number of shared publications:
Hao Wu
School of Public Health, Jilin University, Changchun, Jilin, China; Jilin Guojian Life Engineering Science and Technology Co., Ltd, Changchun, Jilin, China
2 shared publicationsYaoqi Zhu
Department of Stomatology, TaikangTongji Hospital, Wuhan 430000, Hubei Province, P. R. China
2 shared publications- Ali Hou
National Engineering Laboratory for AIDS Vaccine, School of Life Sciences, Jilin University, Changchun 130012, China
1 shared publication Cai Lei Jiang
Institute of Regenerative and Translational Medicine, Tianyou Hospital of Wuhan University of Science and Technology, Wuhan, Hubei, China
1 shared publication- Chao Wang
The State Key Laboratory of Virology, Department of Pathogen Biology, School of Basic Medical Sciences, Hubei Province Key Laboratory of Allergy and Immune-related Diseases, Wuhan University, 185 Eastlake Road, Wuhan, 430071, People's Republic of China
1 shared publication - Chaorong Tie
Department of Stomatology, Taikang Tongji Hospital, Wuhan, 430000, Hubei Province, P. R. China
1 shared publication
Latest Publications
- Open Access
- 1 June 2026
- Published by Elsevier in International Dental Journal
- Vol. 76 (4) , 109650
Differential Associations of Human Herpesviruses With Oral Bacteria and Periodontitis Severity: A Cross-Sectional Analysis
- 1 June 2026
- Published by Elsevier in International Dental Journal
- Vol. 76 (4) , 109650
Open AccessDifferential Associations of Human Herpesviruses With Oral Bacteria and Periodontitis Severity: A Cross-Sectional Analysis
- Open Access
- 18 April 2026
- Published by Elsevier in International Dental Journal
- Vol. 76 (3) , 109557
Mesenchymal Stem Cell-Lysate Sustained-Release Nano-Hydrogel Alleviates Spinal Cord Injury by Inhibiting Ferroptosis and Mitochondrial Intrinsic Apoptosis
- 18 April 2026
- Published by Elsevier in International Dental Journal
- Vol. 76 (3) , 109557
Open AccessMesenchymal Stem Cell-Lysate Sustained-Release Nano-Hydrogel Alleviates Spinal Cord Injury by Inhibiting Ferroptosis and Mitochondrial Intrinsic Apoptosis
- 4 October 2025
- Published by Elsevier in Tissue and Cell
- Vol. 98, 103175
Dental pulp stem cell-derived exosomes promote axonal repair in spinal cord injury by suppressing neuroinflammation and apoptosis
- 4 October 2025
- Published by Elsevier in Tissue and Cell
- Vol. 98, 103175
Dental pulp stem cell-derived exosomes promote axonal repair in spinal cord injury by suppressing neuroinflammation and apoptosis
- Open Access
- 1 February 2021
- Published by Impact Journals, LLC in Aging
- Vol. 13 (4) , 5312-5331
Evaluation of the prognostic values of solute carrier (SLC) family 39 genes for patients with lung adenocarcinoma
Lung cancer is the first fatality rate of cancer-related death worldwide. This study aimed to evaluate the solute carrier family 39 (SLC39A) genes as biological markers associated with the prognosis of lung adenocarcinoma (LUAD). MRNA expression of SLC39A genes in non-small cell lung cancer (NSCLC) was analyzed using UCSC database. We investigated the overall survival (OS) of SLC39A genes in patients with NSCLC as the only prognostic indicator using the Kaplan-Meier plotter. CERES score obtained from the Project Achilles was used to perform the survival analysis. Crystal violet-glutaraldehyde solution staining and CCK-8 assay were used to determine colony formation and cell viability, respectively. For patients with lung squamous cell carcinoma, only high expression of SLC39A3, SLC39A4 and SLC39A7 have significant affections to the prognosis. But for patients with LUAD, 11 out of 14 SLC39A genes were significantly associated with prognostic values. Additional analysis indicated that SLC39A7 played an essential role for cell survival of LUAD. Furthermore, SLC39A7 high expression in LUAD was associated with current smoking. Our findings indicated that SLC39A groups were significantly associated with prognosis of LUAD. The SLC39A7 gene was significantly linked with survival and growth of LUAD cells.
- 1 February 2021
- Published by Impact Journals, LLC in Aging
- Vol. 13 (4) , 5312-5331
Open AccessEvaluation of the prognostic values of solute carrier (SLC) family 39 genes for patients with lung adenocarcinoma
Lung cancer is the first fatality rate of cancer-related death worldwide. This study aimed to evaluate the solute carrier family 39 (SLC39A) genes as biological markers associated with the prognosis of lung adenocarcinoma (LUAD). MRNA expression of SLC39A genes in non-small cell lung cancer (NSCLC) was analyzed using UCSC database. We investigated the overall survival (OS) of SLC39A genes in patients with NSCLC as the only prognostic indicator using the Kaplan-Meier plotter. CERES score obtained from the Project Achilles was used to perform the survival analysis. Crystal violet-glutaraldehyde solution staining and CCK-8 assay were used to determine colony formation and cell viability, respectively. For patients with lung squamous cell carcinoma, only high expression of SLC39A3, SLC39A4 and SLC39A7 have significant affections to the prognosis. But for patients with LUAD, 11 out of 14 SLC39A genes were significantly associated with prognostic values. Additional analysis indicated that SLC39A7 played an essential role for cell survival of LUAD. Furthermore, SLC39A7 high expression in LUAD was associated with current smoking. Our findings indicated that SLC39A groups were significantly associated with prognosis of LUAD. The SLC39A7 gene was significantly linked with survival and growth of LUAD cells.
- 4 October 2019
- Published by Spandidos Publications in International Journal of Oncology
- Vol. 56 (1) , 273-282
Baicalein inhibits the growth of oral squamous cell carcinoma cells by downregulating the expression of transcription factor Sp1
Oral squamous cell carcinoma (OSCC), the most common malignancy of the oral cavity, accounts for >90% of all diagnosed oral cancer cases. Baicalein, a naturally derived compound, has been shown to alter p65 and the nuclear factor (NF)-kappa B pathway, thus exerting cytotoxic effects on various tumor cell types. However, the mechanism of action of baicalein in OSCC has not been fully elucidated. In the present study, the proliferation of OSCC cells treated with baicalein was examined using a CCK-8 assay. The effects of baicalein on the cell cycle and apoptosis of OSCC cells were determined by flow cytometric analyses. The expression of specificity protein 1 (Sp1), p65 and p50 at the mRNA and protein levels was determined by reverse transcription-quantitative PCR and western blot analysis, respectively. The results of the present study demonstrated that baicalein suppresses the proliferation of OSCC cell lines in vivo and in vitro. Baicalein also induced apoptosis of OSCC cells and arrested the cell cycle at the G0/G1 phase. Baicalein inhibited the expression of Sp1, p65 and p50 by downregulating the relative mRNA levels. Baicalein reduced the activity of NF-kappa B in OSCC cells. Knockdown of Sp1 also resulted in reduced expression of p65 and p50. In addition, Sp1 silencing enhanced the effects of baicalein. In conclusion, the present study demonstrated that baicalein suppresses the growth of OSCC cells through an Sp1/NF-kappa B-dependent mechanism.
- 4 October 2019
- Published by Spandidos Publications in International Journal of Oncology
- Vol. 56 (1) , 273-282
Baicalein inhibits the growth of oral squamous cell carcinoma cells by downregulating the expression of transcription factor Sp1
Oral squamous cell carcinoma (OSCC), the most common malignancy of the oral cavity, accounts for >90% of all diagnosed oral cancer cases. Baicalein, a naturally derived compound, has been shown to alter p65 and the nuclear factor (NF)-kappa B pathway, thus exerting cytotoxic effects on various tumor cell types. However, the mechanism of action of baicalein in OSCC has not been fully elucidated. In the present study, the proliferation of OSCC cells treated with baicalein was examined using a CCK-8 assay. The effects of baicalein on the cell cycle and apoptosis of OSCC cells were determined by flow cytometric analyses. The expression of specificity protein 1 (Sp1), p65 and p50 at the mRNA and protein levels was determined by reverse transcription-quantitative PCR and western blot analysis, respectively. The results of the present study demonstrated that baicalein suppresses the proliferation of OSCC cell lines in vivo and in vitro. Baicalein also induced apoptosis of OSCC cells and arrested the cell cycle at the G0/G1 phase. Baicalein inhibited the expression of Sp1, p65 and p50 by downregulating the relative mRNA levels. Baicalein reduced the activity of NF-kappa B in OSCC cells. Knockdown of Sp1 also resulted in reduced expression of p65 and p50. In addition, Sp1 silencing enhanced the effects of baicalein. In conclusion, the present study demonstrated that baicalein suppresses the growth of OSCC cells through an Sp1/NF-kappa B-dependent mechanism.
- Open Access
- 1 September 2018
- Published by Wolters Kluwer Health in Medicine
- Vol. 97 (37) , e12282
Associations of the risk of lung cancer with serum 25-hydroxyvitamin D level and dietary vitamin D intake
The associations of the risk of lung cancer with the vitamin D intake and serum level are controversial. We performed a comprehensive dose-response meta-analysis to evaluate the precise relationships between the above mentioned parameters. We performed a web search of the PubMed, Medline, and Embase databases to identify potential studies that evaluated the relationships between vitamin D intake or serum 25-hydroxyvitamin D (25([OH]D) levels and the risk of lung cancer on December 5, 2017. According to the inclusion and exclusive criteria, 16 studies were included in this meta-analysis. The pooled relative risks (RRs) with 95% confidence intervals (CIs) were used to assess the strength of the associations. A dose-response analysis was conducted to quantitate the relationship between the serum 25(OH)D or vitamin D intake and the risk of lung cancer. The pooled RR (highest level vs lowest level) showed that the serum 25(OH)D level was not associated with the risk of lung cancer (RR = 1.046, 95% CI = 0.945–1.159). A high vitamin D intake was inversely correlated with the lung cancer risk (RR = 0.854, 95% CI = 0.741–0.984). No significant dose-response relationship was observed between the serum 25(OH)D level and the lung cancer risk. The linearity model of the dose-response analysis indicated that with every 100 IU/day increase in vitamin D intake, the risk of lung cancer decreased by 2.4% (RR = 0.976, 95% CI = 0.957–0.995, P = .018). A high vitamin D intake provides limited protection against lung cancer carcinogenesis.
- 1 September 2018
- Published by Wolters Kluwer Health in Medicine
- Vol. 97 (37) , e12282
Open AccessAssociations of the risk of lung cancer with serum 25-hydroxyvitamin D level and dietary vitamin D intake
The associations of the risk of lung cancer with the vitamin D intake and serum level are controversial. We performed a comprehensive dose-response meta-analysis to evaluate the precise relationships between the above mentioned parameters. We performed a web search of the PubMed, Medline, and Embase databases to identify potential studies that evaluated the relationships between vitamin D intake or serum 25-hydroxyvitamin D (25([OH]D) levels and the risk of lung cancer on December 5, 2017. According to the inclusion and exclusive criteria, 16 studies were included in this meta-analysis. The pooled relative risks (RRs) with 95% confidence intervals (CIs) were used to assess the strength of the associations. A dose-response analysis was conducted to quantitate the relationship between the serum 25(OH)D or vitamin D intake and the risk of lung cancer. The pooled RR (highest level vs lowest level) showed that the serum 25(OH)D level was not associated with the risk of lung cancer (RR = 1.046, 95% CI = 0.945–1.159). A high vitamin D intake was inversely correlated with the lung cancer risk (RR = 0.854, 95% CI = 0.741–0.984). No significant dose-response relationship was observed between the serum 25(OH)D level and the lung cancer risk. The linearity model of the dose-response analysis indicated that with every 100 IU/day increase in vitamin D intake, the risk of lung cancer decreased by 2.4% (RR = 0.976, 95% CI = 0.957–0.995, P = .018). A high vitamin D intake provides limited protection against lung cancer carcinogenesis.
- Open Access
- 15 August 2018
- Published by Springer Nature in Journal of Experimental & Clinical Cancer Research
- Vol. 37 (1) , 192
Triptolide inhibits Epstein-Barr nuclear antigen 1 expression by increasing sensitivity of mitochondria apoptosis of nasopharyngeal carcinoma cells
Epstein-Barr virus (EBV) is widely found in nasopharyngeal carcinoma (NPC) tissue and associated with poor prognosis of patients. EBV nuclear antigen 1 (EBNA1) is expressed in all NPC tumors and plays multiple biological roles in both virus and host cells. Triptolide is a natural product extracted from Tripterygium and shows anti-cancer activities. The goal of this work was to illustrate the anti-cancer effect of triptolide and elucidate a novel anti-apoptotic mechanism of EBNA1 in NPC cells encountered with triptolide. In the present study, a CCK-8 assay was used to analyze the proliferation of NPC cells treated with triptolide in a dose- and time-dependent ways. Effects of triptolide on NPC cell cycle and apoptosis were investigated by flow cytometric analysis. EBNA1 expression in mRNA and protein levels was determined by quantitative real-time PCR and Western blot, respectively. Our results showed that triptolide effectively inhibited proliferation of NPC cells. Triptolide arrested NPC cell cycles in S phase and induced apoptosis through a caspase-9-dependent apoptosis pathway. Low-dose of triptolide reduced the half-life of EBNA1 and significantly decreased EBNA1 expression by promoting the process of proteasome-ubiquitin pathway. Over-expression of EBNA1, which was independent from EBV genome, effectively attenuated the apoptosis induced by triptolide. In addition, triptolide significantly inhibited proliferations of tumors induced by EBV-positive cells in vivo. Furthermore, EBNA1 were expressed in all NPC biopsies of Chinese patients. In summary, our study provides the evidence that triptolide induces EBNA1 degradation and stimulates NPC apoptosis through mitochondria apoptotic pathway. In addition, EBNA1 assists NPC cells to resist triptolide-induced apoptosis through inhibiting caspase-9-dependent apoptotic pathway.
- 15 August 2018
- Published by Springer Nature in Journal of Experimental & Clinical Cancer Research
- Vol. 37 (1) , 192
Open AccessTriptolide inhibits Epstein-Barr nuclear antigen 1 expression by increasing sensitivity of mitochondria apoptosis of nasopharyngeal carcinoma cells
Epstein-Barr virus (EBV) is widely found in nasopharyngeal carcinoma (NPC) tissue and associated with poor prognosis of patients. EBV nuclear antigen 1 (EBNA1) is expressed in all NPC tumors and plays multiple biological roles in both virus and host cells. Triptolide is a natural product extracted from Tripterygium and shows anti-cancer activities. The goal of this work was to illustrate the anti-cancer effect of triptolide and elucidate a novel anti-apoptotic mechanism of EBNA1 in NPC cells encountered with triptolide. In the present study, a CCK-8 assay was used to analyze the proliferation of NPC cells treated with triptolide in a dose- and time-dependent ways. Effects of triptolide on NPC cell cycle and apoptosis were investigated by flow cytometric analysis. EBNA1 expression in mRNA and protein levels was determined by quantitative real-time PCR and Western blot, respectively. Our results showed that triptolide effectively inhibited proliferation of NPC cells. Triptolide arrested NPC cell cycles in S phase and induced apoptosis through a caspase-9-dependent apoptosis pathway. Low-dose of triptolide reduced the half-life of EBNA1 and significantly decreased EBNA1 expression by promoting the process of proteasome-ubiquitin pathway. Over-expression of EBNA1, which was independent from EBV genome, effectively attenuated the apoptosis induced by triptolide. In addition, triptolide significantly inhibited proliferations of tumors induced by EBV-positive cells in vivo. Furthermore, EBNA1 were expressed in all NPC biopsies of Chinese patients. In summary, our study provides the evidence that triptolide induces EBNA1 degradation and stimulates NPC apoptosis through mitochondria apoptotic pathway. In addition, EBNA1 assists NPC cells to resist triptolide-induced apoptosis through inhibiting caspase-9-dependent apoptotic pathway.
- Open Access
- 28 June 2017
- Published by Impact Journals, LLC in Oncotarget
- Vol. 8 (49) , 86828-86842
Associations between dietary folate intake and risks of esophageal, gastric and pancreatic cancers: an overall and dose-response meta-analysis
Associations between dietary folate intake and risks of esophageal, gastric and pancreatic cancers: an overall and dose-response meta-analysis Associations between dietary folate intake and risks of esophageal, gastric and pancreatic cancers: an overall and dose-response meta-analysis
- 28 June 2017
- Published by Impact Journals, LLC in Oncotarget
- Vol. 8 (49) , 86828-86842
Open AccessAssociations between dietary folate intake and risks of esophageal, gastric and pancreatic cancers: an overall and dose-response meta-analysis
Associations between dietary folate intake and risks of esophageal, gastric and pancreatic cancers: an overall and dose-response meta-analysis Associations between dietary folate intake and risks of esophageal, gastric and pancreatic cancers: an overall and dose-response meta-analysis