Publications by authors named "Renba Liang"

16 Publications

  • Page 1 of 1

Letter to the editor regarding "XPO1 inhibition synergizes with PARP1 inhibition in small cell lung cancer by targeting nuclear transport of FOXO3a".

Authors:
Renba Liang

Cancer Lett 2021 Oct 23. Epub 2021 Oct 23.

Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, 518116, China. Electronic address:

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.canlet.2021.10.026DOI Listing
October 2021

Letter to the editor regarding "Cedrol suppresses glioblastoma progression by triggering DNA damage and blocking nuclear translocation of the androgen receptor".

Authors:
Renba Liang

Cancer Lett 2021 Oct 9;523:148. Epub 2021 Oct 9.

Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, 518116, China. Electronic address:

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.canlet.2021.10.007DOI Listing
October 2021

Prognostic Role of EGFR/p-EGFR in Patients With Nasopharyngeal Carcinoma: A Meta-Analysis.

Front Oncol 2021 19;11:697369. Epub 2021 Aug 19.

Department of Oncology, Wuming Hospital of Guangxi Medical University, Nanning, China.

Background: The prognostic value of epidermal growth factor receptor (EGFR)/phosphorylated EGFR (p-EGFR) expression in nasopharyngeal carcinoma remains controversial. A meta-analysis was performed to investigate prognostic significance of EGFR/p-EGFR expression in patients with nasopharyngeal carcinoma.

Methods: Literatures published before November 2020 were systematically searched in relevant databases, including PubMed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), and Wan fang databases. STATA 13 statistical software was used to analyze the pooled hazard ratio (HR) and 95% confidence interval (CI). Heterogeneity of the studies was examined by I. Sensitivity and subgroup analysis were performed to explore sources of heterogeneity. The potential publication bias was assessed using both Egger's and Begg's tests.

Results: A total of 20 literatures with 1545 patients were included for the meta-analysis. The meta-analysis results suggested that high expression of EGFR was significantly associated with poor overall survival (OS) (HR = 1.70, 95% CI: 1.24-3.15, P = 0.001) and disease-free survival (DFS) (HR = 2.58, 95% CI: 1.87-3.56, P = 0.000). However, it was not significantly associated with progression-free survival (PFS) (HR = 1.85, 95% CI: 0.90-3.82, P = 0.09) and distant metastasis-free survival (DMFS) (HR = 1.39, 95% CI: 0.73-2.67, P = 0.319). The subgroup analysis indicated that patients with EGFR high expression in studies of higher TNM stage (III-IV) ratio had significantly poor OS (HR = 2.27, 95% CI: 1.09-4.73, P = 0.03), but heterogeneity existed in studies (I  =  95.1%, P = 0.000). Sensitivity analyses revealed that EGFR expression did not significantly affect OS by an individual study solely, indicating there was inherent heterogeneity in OS cohorts. There was no significant heterogeneity among eight studies in the DFS cohorts (I = 0%, P = 0.606). There was significant heterogeneity between EGFR expression and DMFS (I = 82.8%, P = 0.000). Sub-group analysis in differentiated carcinoma demonstrated a smaller heterogeneity (I = 33.2%). In addition, p-EGFR high expression had no significant correlation with OS (HR = 1.00, 95% CI: 0.88-1.14, P = 0.982) and DMFS (HR = 1.21, 95% CI: 0.96-1.52, P = 0.112). The heterogeneity among p-EGFR and OS studies was small (I = 21%, P = 0.26). There was no significant heterogeneity in the DMFS cohorts (I = 0%, P = 0.497).

Conclusion: EGFR high-expression was significantly associated with poor OS and DFS, which may serve as a prognostic predictor for nasopharyngeal cancer.

Systematic Review Registration: [https://www.crd.york.ac.uk/PROSPERO], identifier [number CRD42021258457].
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fonc.2021.697369DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8417403PMC
August 2021

Letter to the editor regarding "Marchantin A, a cyclic bis(bibenzyl ether), isolated from the liverwort Marchantia emarginata subsp. tosana induces apoptosis in human MCF-7 breast cancer cells".

Authors:
Renba Liang

Cancer Lett 2021 Sep 2;521:237. Epub 2021 Sep 2.

Department of Radiation Oncology, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital & Shenzhen Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Shenzhen, 518116, China. Electronic address:

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.canlet.2021.08.040DOI Listing
September 2021

Commentary: Identification of IFN-Induced Transmembrane Protein 1 With Prognostic Value in Pancreatic Cancer Using Network Module-Based Analysis.

Front Oncol 2021 20;11:707516. Epub 2021 Jul 20.

Department of Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3389/fonc.2021.707516DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8329442PMC
July 2021

Nimotuzumab, an Anti-EGFR Monoclonal Antibody, in the Treatment of Nasopharyngeal Carcinoma.

Cancer Control 2021 Jan-Dec;28:1073274821989301

Department of Oncology, Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, People's Republic of China.

Epidermal growth factor receptor (EGFR) is highly expressed in most of Nasopharyngeal carcinoma (NPC) samples and is associated with poor outcomes. Therefore, targeting EGFR may be a promising strategy to improve patient prognosis. Nimotuzumab is a humanized anti-EGFR monoclonal antibody. Recently, accumulating evidence has demonstrated that combination nimotuzumab and induction chemotherapy, radiotherapy, or concurrent chemoradiotherapy confer benefits for patients with NPC. Moreover, the side effects of such regimes are tolerable. In this review, we focus on the current data of nimotuzumab in clinical trials in the treatment of NPC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1177/1073274821989301DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8482709PMC
September 2021

UC2288 induces cell apoptosis of nasopharyngeal carcinoma cells via inhibiting EGFR/ERK pathway.

J Cancer 2021 1;12(4):988-995. Epub 2021 Jan 1.

Department of Oncology, Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, P.R. China.

Radiotherapy and chemotherapy are the standard care for patients with nasopharyngeal carcinoma (NPC). These treatments cause some severe toxicity and about 30% of patients develop recurrence and metastases after treatment. UC2288 is structurally similar to sorafenib, a multikinase inhibitor. However, studies about the effects of UC2288 on tumors are few. Here, UC2288 inhibited proliferation and induced apoptosis of NPC cells in a dose- and time-dependent manner. Using western blot and immunofluorescence assay, we found that UC2288 promoted DNA damage. In addition, UC2288 decreased the phosphorylation of EGFR and ERK. Moreover, pretreatment with EGF partially rescued cell viability suppressed by UC2288. In conclusion, UC2288 suppressed the growth of NPC via inhibiting EGFR/ERK pathway and it may be a promising therapeutic option for NPC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.7150/jca.48282DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7797659PMC
January 2021

CD166 promotes cancer stem cell-like phenotype via the EGFR/ERK1/2 pathway in the nasopharyngeal carcinoma cell line CNE-2R.

Life Sci 2021 Feb 29;267:118983. Epub 2020 Dec 29.

Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, PR China; Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, PR China; Key Laboratory of Early Prevention and Treatment for Regional High-Incidence-Tumor, Guangxi Medical University, Ministry of Education, Nanning, Guangxi, PR China. Electronic address:

Aims: The present study aimed to investigate the role and underlying mechanisms of CD166 in cancer stem cell-like (CSCs) phenotype of the radioresistant nasopharyngeal carcinoma cell CNE-2R.

Main Methods: Established CD166-shRNA- CNE-2R cell line by lentivirus-mediated silencing CD166. Then, CSC-related genes mRNAs and proteins, and EGFR/ERK1/2 signaling pathway were detected using RT-PCR and western blot. Sphere formation assay was performed to evaluate the sphere formation capacity in CD166-shRNA- CNE-2R cells. The tumorigenesis ability in vivo was examined in nude mice mode.

Key Findings: Downregulation of CD166 inhibited the expression of the CSC-related genes, pEGFR and pERK in vitro and vivo. The capacity to form spheres and tumorigenesis was significantly decreased in CD166-shRNA cells. Furthermore, EGF-stimulated CD166-shRNA cells exhibited an increase in CSC-like traits by activating EGFR/ERK1/2 signaling.

Significance: CD166 induced CSCs formation by activating the EGFR/ERK1/2 signaling pathway in nasopharyngeal carcinoma, which may serve as a critical molecular target for NPC therapeutic strategies.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.lfs.2020.118983DOI Listing
February 2021

VEGF promotes migration and invasion by regulating EMT and MMPs in nasopharyngeal carcinoma.

J Cancer 2020 21;11(24):7291-7301. Epub 2020 Oct 21.

Department of Oncology, Affiliated Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, 530010, People's Republic of China.

Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. Accumulating data have indicated that VEGF is involved in tumour metastasis. However, the mechanism through which VEGF regulates nasopharyngeal carcinoma (NPC) metastasis is largely unknown. This study aimed to examine the biological function of VEGF in NPC metastasis and its underlying mechanism. We used western blotting and qPCR to examine the difference in VEGF expression between NPC cells and the immortalized nasopharyngeal epithelial cell line NP69. Wound healing assays, transwell assays and animal experiments were used to further verify the role of VEGF in the invasion and migration of NPC cells. The protein levels of the epithelial-mesenchymal transition (EMT) and matrix metalloproteinase (MMP) family were analysed by immunofluorescence (IF) and western blotting. Enzyme-linked immunosorbent assay (ELISA) and transwell assays were used to determine whether VEGF enhanced the invasion and migration of NPC cells in an autocrine manner. Western blotting was used to examine how autocrine VEGF-VEGFR2 signalling regulated EMT and MMPs. We observed higher levels of VEGF in NPC cells than that in NP69 cells and identified an association between high VEGF levels and tumour invasion and migration. Mechanistically, the VEGF-mediated increase in EMT markers, MMP2 and MMP9 promoted NPC cell invasion and migration Additionally, NPC cells secreted VEGF to promote cell invasion, migration and angiogenesis. Autocrine VEGF-VEGFR2 signalling increased ERK1/2 phosphorylation, promoted EMT process and MMPs at the indicated times. This study revealed that VEGF plays a role in controlling NPC cell metastasis by regulating EMT markers and MMPs in an autocrine manner.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.7150/jca.46429DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7646165PMC
October 2020

Comment on: an orally antitumor chalcone hybrid inhibited HepG2 cells growth and migration as the tubulin binding agent.

Invest New Drugs 2021 04 29;39(2):537. Epub 2020 Oct 29.

Department of Oncology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, China.

Recently we read a paper in Investigational New Drugs "An orally antitumor chalcone hybrid inhibited HepG2 cells growth and migration as the tubulin binding agent". Chalcone hybrid 9, a novel chalcone derivative, may be a promising agent for the treatment of hepatocellular carcinoma. However, there are some problems in this paper that are worthy of comment. Human hepatocellular carcinoma HepG2 cells from Shanghai Research Science Limited Company could generate xenograft in nude mice and chalcone hybrid 9 suppressed the growth of HepG2 tumor. However, according to the description of cell bank of Chinese Academy of Science and ATCC, HepG2 cells are no tumorigenic. Similarly, our lab also confirmed that HepG2 cells cannot demonstrate tumorigenic ability in nude mice. Therefore, this discrepancy raised our concern about HepG2 xenograft in the paper.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10637-020-01026-wDOI Listing
April 2021

VEGF knockdown enhances radiosensitivity of nasopharyngeal carcinoma by inhibiting autophagy through the activation of mTOR pathway.

Sci Rep 2020 10 1;10(1):16328. Epub 2020 Oct 1.

Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, 530021, Guangxi, People's Republic of China.

Vascular endothelial growth factor (VEGF) is an important pro-angiogenic factor. VEGF was reported to promote the occurrence of autophagy, which enhanced the radioresistance of tumors. The purpose of this study was to investigate the influence of VEGF silencing on the radiosensitivity of nasopharyngeal carcinoma (NPC) cells and the underlying mechanisms. The radiosensitivity of NPC cells after VEGF silencing was detected by cell counting kit 8 (CCK-8) and clonogenic assay, while cell cycle and apoptosis were detected by flow cytometry. The processes of DNA damage, repair and autophagy were examined by immunofluorescence and western blotting. The interaction between VEGF and mTOR was confirmed by western blotting and co-immunoprecipitation studies. The effect of VEGF on radiosensitivity of NPC cells was investigated in vivo using a xenograft model. Furthermore, immunohistochemistry and TUNEL assays were used to verify the relationship between autophagy and radiosensitivity in NPC after VEGF depletion. Downregulation of VEGF significantly inhibited cell proliferation and induced apoptosis of NPC cells after radiotherapy in vitro and in vivo. In addition, VEGF knockdown not only decreased autophagy level, but also delayed the DNA damage repair in NPC cells after irradiation. Mechanistically, silencing VEGF suppressed autophagy through activation of the mTOR pathway. VEGF depletion increased radiosensitivity of NPC cells by suppressing autophagy via activation of the mTOR pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1038/s41598-020-73310-xDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7531011PMC
October 2020

Anti-EGFR therapies in nasopharyngeal carcinoma.

Biomed Pharmacother 2020 Nov 21;131:110649. Epub 2020 Aug 21.

Wuming Hospital of Guangxi Medical University, Nanning, Guangxi, PR China; Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, PR China; Key Laboratory of Early Prevention and Treatment for Regional High-Incidence-Tumor, Guangxi Medical University, Ministry of Education, Nanning, Guangxi, PR China. Electronic address:

Nasopharyngeal carcinoma (NPC) is a common malignant tumor in Southern China and South-East Asia. Regardless of initiative high response to radiotherapy, parts of patients still have relapses and metastases. It is reported that epidermal growth factor receptor (EGFR) is highly expressed in most of NPC and is a poor prognostic factor. Targeting EGFR therapies including monoclonal antibodies and EGFR tyrosine kinase inhibitors (EGFR-TKIs), offer different benefits and toxicities for patients with NPC. Herein, we summarize the clinical evidence of anti-EGFR therapies in the management of NPC and provide a direction for the treatment and research of NPC in the future.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.biopha.2020.110649DOI Listing
November 2020

Letter to the editor Re: Pan et al. "LLY17, a novel small molecule STAT3 inhibitor induces apoptosis and suppresses cell migration and tumor growth in triple-negative breast cancer".

Authors:
Renba Liang

Breast Cancer Res Treat 2020 11 14;184(2):653. Epub 2020 Aug 14.

Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, No. 71 He Di Road, Nanning, 530021, Guangxi, People's Republic of China.

View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s10549-020-05853-6DOI Listing
November 2020

Deciphering the Roles of IFITM1 in Tumors.

Mol Diagn Ther 2020 08;24(4):433-441

Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, P.R. China.

Interferon (IFN)-induced transmembrane protein 1 (IFITM1), a member of the IFN-induced transmembrane protein family, is reported to be highly expressed in tumor tissues as well as cancer cell lines, and it is an independent prognostic biomarker for patients with certain tumor types, such as gallbladder carcinoma, esophageal adenocarcinoma, colorectal cancer, and gastric cancer. Moreover, overexpression of IFITM1 promotes tumor cell proliferation, invasion, metastasis, angiogenesis, and therapeutic resistance, including endocrine therapy, chemotherapy, and radiotherapy resistance. Due to these diverse functions of IFITM1 in tumors, targeting IFITM1 may provide a novel strategy for cancer treatment and be highly desirable to improve cancer patient outcomes. Herein, we decipher the role of IFITM1 in cancer in detail.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1007/s40291-020-00469-4DOI Listing
August 2020

A positive feedback loop between Wnt/β-catenin signaling and hTERT regulates the cancer stem cell-like traits in radioresistant nasopharyngeal carcinoma cells.

J Cell Biochem 2020 11 17;121(11):4612-4622. Epub 2020 Feb 17.

Department of Radiation Oncology, Guangxi Medical University Cancer Hospital, Nanning, Guangxi, China.

Radioresistance may be induced by cancer stem cells (CSCs), while the biological traits of CSCs need to be retained by telomerase. The telomerase activity mainly depends on the transcriptional regulation of human telomerase reverse transcriptase (hTERT). Moreover, Wnt/β-catenin signaling is also considered essential for maintaining the CSC phenotypes. In the previous study, we discovered that the radioresistant nasopharyngeal carcinoma cells CNE-2R displayed CSC-like traits, as well as high expression of hTERT and β-catenin, but whether hTERT and β-catenin were involved in regulating the CSC-like traits and radiosensitivity of CNE-2R cells remained unclear. In this study, our results suggested that hTERT could positively regulate the expression of CSC-related proteins, as well as the cytoplasm- and nucleus-β-catenin, but it could not markedly regulate the expression of total β-catenin in CNE-2R cells. Meanwhile, Wnt/β-catenin signaling had a positive regulatory effect on the expression of hTERT and CSC-related proteins. Moreover, there was a β-catenin/hTERT protein complex in CNE-2R cells, indicating that β-catenin could directly interact with hTERT protein. Our results also revealed that silencing hTERT or suppressing Wnt/β-catenin signaling could attenuate telomerase activity and radioresistance of CNE-2R cells; while suppressing Wnt/β-catenin signaling, the telomerase activity and radioresistance could be reversed through overexpressing hTERT. Taken together, we have outlined a positive feedback loop between Wnt/β-catenin signaling and hTERT in CNE-2R cells, which can regulate the telomerase activity and CSC-like traits, thus regulating the radiosensitivity. Therefore, blocking Wnt/β-catenin signaling transduction and interfering with hTERT expression may be a promising approach for targeting radioresistant nasopharyngeal carcinoma cells with CSC-like traits.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jcb.29681DOI Listing
November 2020

STAT3 signaling in ovarian cancer: a potential therapeutic target.

J Cancer 2020 1;11(4):837-848. Epub 2020 Jan 1.

Department of Radiation Oncology, Guangxi Medical University Cancer Hospital and Cancer Institute of Guangxi Zhuang Autonomous Region, Nanning, Guangxi, P.R. China.

Accumulating evidence has shown that Signal Transducer and Activator of Transcription 3 (STAT3) is thought to be a promising target for cancer therapy as STAT3 is frequently overexpressed in a wide range of cancer cells as well as clinical specimens, promoting tumor progression. It is widely accepted that STAT3 regulates a variety of cellular processes, such as tumor cell growth, survival, invasion, cancer stem cell-like characteristic, angiogenesis and drug-resistance. In this review, we focus on the role of STAT3 in tumorigenesis in ovarian cancer and discuss the existing inhibitors of STAT3 signaling that can be promisingly developed as the strategies for ovarian cancer therapy.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.7150/jca.35011DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6959025PMC
January 2020
-->