Search

Your search keyword '"Le, Kehao"' showing total 17 results
Start Over Author "Le, Kehao"
17 results on '"Le, Kehao"'

11. SRC Promotes Tamoxifen Resistance in Breast Cancer via Up-Regulating SIRT1

Author

Zhou,Jun, Xu,Ming, Le,Kehao, Ming,Jie, Guo,Hui, Ruan,Shengnan, and Huang,Tao

Subjects
skin and connective tissue diseases, hormones, hormone substitutes, and hormone antagonists, OncoTargets and Therapy
Abstract

Jun Zhou,* Ming Xu,* Kehao Le, Jie Ming, Hui Guo, Shengnan Ruan, Tao Huang Department of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, People’s Republic of China*These authors contributed equally to this workCorrespondence: Tao Huang; Shengnan RuanDepartment of Breast and Thyroid Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, People’s Republic of ChinaTel +86-27-85351622Email huangtaowh@163.com; ruanshengnan@yahoo.comBackground: Endocrine therapy plays a key role in estrogen receptor-positive breast cancer patients; but, tamoxifen resistance could be a real difficulty for these patients. Several attempts have been made to explore the mechanism and new therapies for these patients. We intend to clarify the expression change of SRC and SIRT1 in tamoxifen-resistant breast cancer cells and explore their functions on tamoxifen resistance.Methods: SRC and SIRT1 expressions were analyzed by RNA sequencing, qPCR and Western blotting. Loss and gain of function of SRC and SIRT1 were utilized to indicate their oncogenic roles in tamoxifen resistance in vitro and in vivo. Kaplan–Meier analysis and receiver operating characteristic curve were used to evaluate the survival and the predicted effects of SRC and SIRT1 on patients’ prognosis.Results: High expressions of SRC and/or SIRT1 were found in tamoxifen-resistant cells and related to poor overall survival (p< 0.05 for SRC, p< 0.001 for SIRT1, p< 0.001 for SRC and SIRT1) and cancer-specific survival (p< 0.05 for SRC, p< 0.01 for SIRT1, p< 0.01 for SRC and SIRT1) of tamoxifen-treated breast cancer patients. Down-regulation of SRC (p< 0.01) or SIRT1 (p< 0.05) separately reversed the resistance to tamoxifen and the minimal concentration of SRC inhibitor KX-01 (p< 0.05) or SIRT1 inhibitor EX527 (p< 0.001) could also suppress cell proliferation. The expression level of SIRT1 was positively correlated with that of SRC. Overexpression of SRC significantly promotes the cell resistance to tamoxifen inhibited by SIRT1 (p< 0.01). In vivo experiments confirmed the effects of SRC on tumor growth by over- or down-regulating SRC expression (p< 0.001 and p< 0.001, respectively).Conclusion: SRC and SIRT1 are both up-regulated in tamoxifen-resistant breast cancer cells and related to a poor prognosis in tamoxifen-treated breast cancer. Moreover, SRC could promote tamoxifen resistance by up-regulating SIRT1. SRC and SIRT1 might be novel therapeutic targets in tamoxifen-resistant breast cancer and the interaction between SRC and SIRT1 needs to be further explored.Keywords: breast cancer, tamoxifen resistance, SRC, SIRT1, inhibitor

Published
2020

17. Tumor growth manifested in two-fifths of low-risk papillary thyroid microcarcinoma patients during active surveillance: data from a tertiary center in China.

Author

Le K, Jin L, Zhong F, Huang X, Zhou L, Zhou J, and Xie L

Subjects
Aged, Humans, Middle Aged, Risk, Watchful Waiting, China, Young Adult, Adult, Carcinoma, Papillary epidemiology, Carcinoma, Papillary pathology, Thyroid Neoplasms pathology
Abstract

Purpose: To assess tumor growth using tumor doubling rate (TDR) during active surveillance (AS) in China., Methods: Between January 2016 and June 2020, a total of 219 patients with low-risk papillary thyroid microcarcinoma (PTMC) (aged 23-75 years) were consecutively enrolled in the AS program., Results: Four sections of TDR, >0.5, 0.1~0.5, -0.1~0.1 and <-0.1, corresponded with four categories of tumor volume kinetics: rapid growth, slow growth, stable, and decreased size. We found that 10.5% of PTMCs exhibited rapid growth, 33.33% exhibited slow growth, 26.48% were stable, and 29.68% decreased in size. Tumor growth was associated with two factors: age and volume of PTMC at diagnosis. 85.72% of elderly patients (≥ 61 years old) had tumors that remained stable or even shrank and rapidly growing tumors were not found in them. When the volume was small (≤14.13 mm 3 ), the proportion of rapid growth was high (41.67%), whereas when the volume was large (> 179.5 mm 3 ), the proportion of non-growth was 68.75%., Conclusion: TDR may be a better metric for evaluating tumor growth in observational PTMCs. A certain proportion of PTMCs grow during the period of AS and tumor growth was associated with age and volume of PTMC at initial diagnosis. Therefore, how to block tumor growth during the AS period, especially for young patients and patients with early-stage PTMC (size ≤ 5 mm), will be a new challenge., Competing Interests: Author JZ was employed by Hangzhou KuaikuaiKangfu Technology Co., LTD. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Le, Jin, Zhong, Huang, Zhou, Zhou and Xie.)

Published
2024
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results