Publications by authors named "Wei-Bing Zhou"

8 Publications

  • Page 1 of 1

Long Noncoding RNA GAS5 Targeting miR-221-3p/Cyclin-Dependent Kinase Inhibitor 2B Axis Regulates Follicular Thyroid Carcinoma Cell Cycle and Proliferation.

Pathobiology 2021 15;88(4):289-300. Epub 2021 Jun 15.

Department of Oncology, Xiangya Hospital, Central South University, Changsha, China.

Introduction: Follicular thyroid carcinoma (FTC) is more aggressive than the most common papillary thyroid carcinoma (PTC). However, the current research on FTC is less than PTC. Here, we investigated the effects of long noncoding RNA (lncRNA) GAS5 and miR-221-3p in FTC.

Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to detect GAS5 and miR-221-3p expression in the FTC tissues and cells. Cell proliferation was assessed by CCK8 and EdU assays. Flow cytometry was performed to determine the cell cycle. The dual-luciferase reporter assay was employed to validate the binding relationship of GAS5/miR-221-3p and miR-221-3p/cyclin-dependent kinase inhibitor 2B (CDKN2B). Western blot was conducted to measure the protein level of CDKN2B.

Results: Our results displayed that GAS5 was downregulated, while miR-221-3p was upregulated in FTC tissues and cells. What's more, overexpression of GAS5 or miR-221-3p inhibition induced G0/G1 phase arrest and inhibited cell proliferation of FTC cells. GAS5 acted as a sponge of miR-221-3p, and CDKN2B was a target gene of miR-221-3p. Additionally, GAS5 inhibited cell cycle and proliferation of FTC cells via reducing miR-221-3p expression to enhance CDKN2B expression.

Conclusion: GAS5 induced G0/G1 phase arrest and inhibited cell proliferation via targeting miR-221-3p/CDKN2B axis in FTC. Thus, GAS5 may be a potential therapeutic target for the treatment of FTC.
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http://dx.doi.org/10.1159/000513338DOI Listing
June 2021

STARD4 promotes breast cancer cell malignancy.

Oncol Rep 2020 Dec 12;44(6):2487-2502. Epub 2020 Oct 12.

Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

Breast cancer (BRCA) is one of the most common malignancies encountered in women worldwide. Lipid metabolism has been found to be involved in cancer progression. Steroidogenic acute regulatory protein‑related lipid transfer 4 (STARD4) is an important cholesterol transporter involved in the regulatory mechanism of intracellular cholesterol homeostasis. However, to the best of our knowledge, the molecular functions of STARD4 in BRCA are unclear. Immunohistochemical staining and public dataset analysis were performed to investigate the expression levels of STARD4 in BRCA. In the present study, high expression of STARD4 was identified in BRCA samples and higher STARD4 expression was significantly associated with shorter distant metastasis‑free survival time in patients with BRCA, which indicated that STARD4 may be associated with BRCA progression. Cell cytometry system Celigo® analysis, Cell Counting K‑8 assays, flow cytometry, wound healing assays and transwell assays were used to investigate the effects of STARD4 knockdown on proliferation, cell cycle, apoptosis and migration in BRCA cells. Loss‑of‑function assays demonstrated that STARD4 acted as an oncogene to promote proliferation and cell cycle progression, while suppressing apoptosis in BRCA cells in vitro and in vivo. Furthermore, knockdown of STARD4 significantly suppressed BRCA metastasis. To assess the mechanism of action of STARD4, microarray analysis was performed following STARD4 knockdown in MDA‑MB‑231 cells. The data were analyzed in detail using bioinformatics, and a series of genes, including E74 like ETS transcription factor 1, cAMP responsive element binding protein 1 and p21 (RAC1) activated kinase 2, which have been previously reported to be crucial genes implicated in the malignant phenotype of cancer cells, were identified to be regulated by STARD4. Loss‑of function assays demonstrated that knockdown of STARD4 suppressed BRCA proliferation and migration. These findings suggested that STARD4 had an oncogenic effect in human BRCA progression.
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http://dx.doi.org/10.3892/or.2020.7802DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7610339PMC
December 2020

ANLN Directly Interacts with RhoA to Promote Doxorubicin Resistance in Breast Cancer Cells.

Cancer Manag Res 2020 7;12:9725-9734. Epub 2020 Oct 7.

Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, People's Republic of China.

Background: Chemotherapy resistance is the leading cause of cancer treatment failure. This research was conducted to explore a potential link between actin-binding protein anillin (ANLN) and doxorubicin resistance in breast cancer.

Materials And Methods: We compared ANLN expression and 50% inhibition concentration (IC50) of doxorubicin in human breast cancer cells (MDA-MB-231) and human breast cancer cells with doxorubicin resistance (MDA-MB-231/ADM). Co-immunoprecipitation was used to investigate the interaction between ANLN and RhoA. The cell viability, apoptosis, gene and protein expression were estimated by MTT, flow cytometry, quantitative real-time PCR and western blot.

Results: The doxorubicin resistance in MDA-MB-231/ADM cells (IC50 = 19.40 ± 1.16 μg/mL) was significantly higher than that in MDA-MB-231 cells (IC50 = 1.65 ± 0.23 μg/mL). ANLN was up-regulated in MDA-MB-231/ADM cells compared to MDA-MB-231 cells. Furthermore, ANLN overexpression promoted cell viability and inhibited apoptosis of MDA-MB-231 cells. The gene and protein expression of multidrug resistance (MDR1) and cancer resistance protein (BCRP) were enhanced by ANLN overexpression in MDA-MB-231 cells. ANLN silencing suppressed cell viability and the expression of MDR1 and BCRP and facilitated apoptosis in MDA-MB-231/ADM cells. Moreover, ANLN promoted RhoA activation by interacting with RhoA. ANLN up-regulation enhanced cell viability and the expression of MDR1 and BCRP and decreased apoptosis of MDA-MB-231 cells. The influence conferred by ANLN overexpression was effectively abolished by C3 transferase.

Conclusion: This work revealed that ANLN promoted doxorubicin resistance in breast cancer cells by activating RhoA. Thus, our study suggests a novel target for breast cancer treatment.
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http://dx.doi.org/10.2147/CMAR.S261828DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7548225PMC
October 2020

LncRNA XIST promotes chemoresistance of breast cancer cells to doxorubicin by sponging miR-200c-3p to upregulate ANLN.

Clin Exp Pharmacol Physiol 2020 08 6;47(8):1464-1472. Epub 2020 May 6.

Department of Oncology, Xiangya Hospital, Central South University, Changsha, China.

The resistance of breast cancer cells to drugs is a major obstacle to effective cancer chemotherapy. Here, we study the function mechanisms of long non-coding RNA XIST in chemoresistance of breast cancer to doxorubicin. We examined the 50% inhibitive concentration of doxorubicin to MDA-MB-231 and MDA-MB-231/ADM cells, showing that the doxorubicin resistance of MDA-MB-231/ADM cells was much higher than MDA-MB-231 cells. The gene or protein expression of XIST and ANLN were also higher in MDA-MB-231/ADM cells than that in MDA-MB-231 cells. Moreover, XIST overexpression promoted cell proliferation and inhibited apoptosis of doxorubicin-treated MDA-MB-231 cells by promoting ANLN expression. XIST silencing inhibited cell proliferation and promoted apoptosis of doxorubicin-treated MDA-MB-231/ADM cells by inhibiting ANLN expression. Luciferase reporter assay showed that XIST functioned as a competing endogenous RNA to repress miR-200c-3p, which controlled its downstream target ANLN. In conclusion, these data reveal that XIST promotes chemoresistance of breast cancer cells to doxorubicin by sponging miR-200c-3p to upregulate ANLN. This work explores the relationship between lncRNA XIST and doxorubicin resistance in breast cancer cells and highlights a novel therapeutic target for the treatment of breast cancer.
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http://dx.doi.org/10.1111/1440-1681.13307DOI Listing
August 2020

Cathepsin L interacts with CDK2-AP1 as a potential predictor of prognosis in patients with breast cancer.

Oncol Lett 2020 Jan 7;19(1):167-176. Epub 2019 Nov 7.

Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

Cathepsin L (CTSL) is a lysosomal acid cysteine protease that has been implicated in tumorigenesis and malignant progression. In the present study, the role of CTSL in tumorigenesis and prognosis of breast cancer was evaluated. The prognostic value of CTSL was analyzed using immunohistochemistry in patients with breast cancer, as well as online microarray datasets. CTSL expression was knocked down in the breast cancer cell line T-47D using RNA interference. MTT and colony formation assays were performed to assess the role of CTSL in the proliferation of breast cancer cells. Cell cycle progression and apoptosis were measured using flow cytometry. A physical interaction of CTSL and cyclin dependent kinase 2 associated protein 1 (CDK2-AP1) was determined using a glutathione S-transferase pull-down assay. Endogenous CTSL expression was high in breast cancer cells and exhibited an inverse association with CDK2-AP1 expression; aberrant expression of CTSL in breast cancer tissues predicted an improved clinical outcome and prognosis. In addition, CTSL knockdown decelerated the progression of breast cancer cells by arresting cell cycle progression and increasing apoptosis. Thus, CTSL may be a potential therapeutic target for treating patients with breast cancer.
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http://dx.doi.org/10.3892/ol.2019.11067DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6924096PMC
January 2020

MTMR3 is upregulated in patients with breast cancer and regulates proliferation, cell cycle progression and autophagy in breast cancer cells.

Oncol Rep 2019 Nov 23;42(5):1915-1923. Epub 2019 Aug 23.

Department of Oncology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, P.R. China.

As a member of the myotubularin family, myotubularin related protein 3 (MTMR3) has been demonstrated to participate in tumor development, including oral and colon cancer. However, little is known about its functional roles in breast cancer. In the present study, the expression of MTMR3 in breast cancer was evaluated by immunohistochemical staining of tumor tissues from 172 patients. Online data was then used for survival analysis from the PROGgeneV2 database. In vitro, MTMR3 expression was silenced in MDA‑MB‑231 cells via lentiviral shRNA transduction. MTT, colony formation and flow cytometry assays were performed in the control and MTMR3‑silenced cells to evaluate the cell growth, proliferation and cell cycle phase distribution, respectively. Western blotting was used to evaluate the protein expression levels of autophagy‑related markers. The results demonstrated that the expression of MTMR3 in breast cancer tissues was significantly increased compared with adjacent normal tissues. MTMR3 was highly expressed in triple‑negative breast cancer and was associated with disease recurrence. MTMR3 knockdown in MDA‑MB‑231 cells inhibited cell proliferation and induced cell cycle arrest and autophagy. The present results indicated that MTMR3 may have an important role in promoting the progression of breast cancer, and its inhibition may serve as a promising therapeutic target for breast cancer treatment.
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http://dx.doi.org/10.3892/or.2019.7292DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6775797PMC
November 2019

Overexpression of ANLN contributed to poor prognosis of anthracycline-based chemotherapy in breast cancer patients.

Cancer Chemother Pharmacol 2017 03 27;79(3):535-543. Epub 2017 Feb 27.

Department of Oncology, Xiangya Hospital, Central South University, Changsha, 410008, People's Republic of China.

Purpose: To investigate the associations of ANLN expression with prognosis of breast cancer and clinical outcome of anthracycline-based chemotherapy.

Methods: This study enrolled 308 breast cancer patients in which 264 of them received anthracycline-based chemotherapy. Immunohistochemistry was used to detect ANLN expression level of the patients. Clinical characteristics of the patients were collected, and associations of ANLN expression with prognosis were analyzed.

Results: Our results showed that ANLN expression was associated with survival of breast cancer patients, and it was also related to clinical outcome of patients received anthracycline-based chemotherapy. Breast cancer patients with high expression of ANLN would have poor prognosis and poor clinical outcome to anthracycline-based chemotherapy.

Conclusion: ANLN could be an independent prognosis predictor for breast cancer, and its expression might be used to predict the anthracycline-based chemotherapy clinical outcome in breast cancer patients.
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http://dx.doi.org/10.1007/s00280-017-3248-2DOI Listing
March 2017

[Radiotherapy for and prognosis of breast cancer patients with local-regional recurrence after mastectomy].

Ai Zheng 2009 Oct;28(10):1077-82

Department of Radiation Oncology, Cancer Hospital, Fudan University, Shanghai 20032, P.R.China.

Background And Objective: Controversies remain regarding the therapeutic principle for and prognosis of breast cancer patients with isolated local-regional recurrence after mastectomy. This study was to evaluate the role of radiotherapy in treating these patients and to investigate the prognosis.

Methods: Clinical data of 255 breast cancer patients with chest-wall and/or regional lymph node recurrence as first failure after mastectomy from 1990 to 2005 were analyzed. All patients received radiotherapy for recurrence.

Results: The median follow-up time was 45 months (9 months-15.5 years). The median disease-free interval (DFI) was 22 months (2-260 months); it was 37 months in patients with positive hormonal receptor and 17 months in those with unknown or negative receptor. The 2-, 5-, and 8-year overall survival (OS) rates were 86.4%, 56.5%, and 35.0%, respectively. The median survival time was 79 months. The 2-, 5-and, 8-year local control rates were 6.1%, 36.3%, and 27.6%, respectively. Univariate prognostic analysis showed that DFI, site and number of recurrence, receptor status, short-term therapeutic response, initial T status and axillary involvement significantly affected the survival (all P<0.05); multivariate analysis showed that DFI, receptor status, site and number of recurrence were independent prognostic factors. Prognostic index was established to classify the patients. The 2-, 5-and 8-year OS rates were 100%, 91.6%, and 56.4% in the favorable prognosis group, 88.1%, 59.1%, and 36.8% in the medium prognosis group, 68.0%, 8.5%, and 0 in the poor prognosis group (P<0.001).

Conclusion: Radiotherapy is effective for breast cancer patients with isolated local-regional recurrence after mastectomy. Prognostic index could be applied to predict the prognosis.
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http://dx.doi.org/10.5732/cjc.008.10538DOI Listing
October 2009
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