Down-regulation of miR-29b in carcinoma associated fibroblasts promotes cell growth and metastasis of breast cancer

Liu, Yonglei; Zhang, Jingling; Sun, Xiaojiang; Su, Qiang; You, Cuiping

doi:10.18632/oncotarget.17136

Cited by 54 publications

(45 citation statements)

References 36 publications

(32 reference statements)

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“…Wu et al hinted that miR-29 functioned as a tumor suppressor in breast cancer cells by down-regulation of B-Myb [29]. Liu et al announced that miR-29b accelerated breast cancer cells cell growth and metastasis [30]. Nonetheless, whether miR-29 affected the biological processes of breast cancer cells under Sino administration remains vague.…”

Section: Discussionmentioning

confidence: 99%

Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis

Gao

Liang

Ma³

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Sinomenine (Sino) is diffusely applied in heal rheumatoid arthritis and neuralgia. Howbeit, the activities of Sino in breast cancer cells remain confused. The research attempted to probe the anti-tumor function of Sino in breast cancer cells and divulge the feasible molecular mechanism. Sion at the 1-16 lM concentrations was exploited for the exposure of MDA-MB-231 or MCF7 cells, and cell growth, migration, invasion, cell cycle-relevant and apoptosis-correlative factors were estimated. Micro RNA (miR)-29 expression was evaluated via enforcing qRT-PCR, and the actions of miR-29 in MDA-MB-231 cells growth, migration and invasion were appraised after the overexpressed or suppressed vectors transfection. The functions of PDCD-4 in JNK and MEK/ERK pathways were estimated by employing western blot. We found that, Sino exposure impeded cell proliferation, provoked cell apoptosis and barricaded cell migration and invasion in MDA-MB-231 and MCF7 cells. Enhancement of miR-29 was observed in Sino-managed cells, and miR-29 overexpression further potentiated the activities of Sino in MDA-MB-231 cells. Additionally, Sino remarkably enhanced PCDC-4 expression via adjusting miR-29 in MDA-MB-231 cells. Beyond that, overexpressed PCDC-4 obstructed JNK and MEK/ERK pathways in MDA-MB-231 cells. Taken together, the explorations unveiled that Sino restrained MDA-MB-231 cells proliferation, migration, invasion, and provoked apoptosis through modulation of miR-29/PDCD-4 axis. HIGHLIGHT 1. Sino inhibits MDA-MB-231 and MCF7 cells proliferation and provokes apoptosis; 2. Sino restrains MDA-MB-231 and MCF7 cells migration and invasion; 3. Sino ascends miR-29 expression in MDA-MB-231 and MCF7 cells; 4. Sino adjusts cell growth, migration and invasion via modulating miR-29; 5. Sino up-regulates PDCD-4 expression through mediating miR-29; 6. PDCD-4 obstructs JNK and MEK/ERK pathways in MDA-MB-231 cells. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis

Gao

Liang

Ma³

2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Furthermore, lower miR-29b expression in CAFs can accelerate metastasis by activating the p38-STAT1 pathway in breast cancer cells and up-regulating CXCL14 and CCL11 in CAFs. Additionally, STAT1 increases expression of CXCL14 and CCL11 at the transcription level [62]. Kaplan-Meier curves revealed that high CXCL14 mRNA levels were correlated with favorable relapse-free survival (RFS) in all types of BC patients, and high transcription levels of CXCL14 conferred an overall survival (OS) advantage in all BC patients.…”

Section: Discussionmentioning

confidence: 99%

Identification of Potential Therapeutic Targets Among CXC Chemokines in Breast Tumor Microenvironment Using Integrative Bioinformatics Analysis

Chen

Qin

Peng

et al. 2018

Cell Physiol Biochem

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Background/Aims: Breast cancer is a common cause of cancer mortality throughout the world. The cross-talk between cancer cells and interstitial cells exerts significant effects on neoplasia and tumor development and is modulated in part by chemokines. CXC is one of four chemokine families involved in mediating survival, angiogenesis, and immunosensitization by chemoattracting leukocytes, and it incentivizes tumor cell growth, invasion and metastasis in the tumor microenvironment. However, the differential expression profiles and prognostic values of these chemokines remains to be elucidated. Methods: In this study, we compared transcriptional CXC chemokines and survival data of patients with breast carcinoma (BC) using the ONCOMINE dataset, Kaplan-Meier Plotter, TCGA and cBioPortal. Results: We discovered increased mRNA levels for CXCL8/10/11/16/17, whereas mRNA expression of CXCL1/2/3/4/5/6/7/12/14 was lower in BC patients compared to non-tumor tissues. Kaplan-Meier plots revealed that high mRNA levels of CXCL1/2/3/4/5/6/7/12/14 correlate with relapse-free survival (RFS) in all types of BC patients. Conversely, high CXCL8/10/11 predicted worse RFS in BC patients. Significantly, high transcription levels of CXCL9/12/13/14 conferred an overall survival (OS) advantage in BC patients, while high levels of CXCL8 demonstrated shorter OS in all BC sufferers. Conclusions: Integrative bioinformatics analysis suggests that CXCL8/12/14 are potential suitable targets for precision therapy in BC patients compared to other CXC chemokines.

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“…Cancer associated fibroblasts (CAF) play an important part in sustaining and protecting tumor cells and may lend themselves to new unconventional approaches to cancer therapy [123]. CAFs co-cultured with breast cancer cells produce high levels of CCL11 and CXCL14 chemokines, which stimulate cancer cell proliferation and resistance to paclitaxel by activating p38 -STAT1 signaling [67,124]. Triple-negative breast cancer often shows overexpression of interleukin-1 receptor-associated kinase 1 (IRAK1), and paclitaxel treatment activates IRAK1, which increases the stemness of cancer cells and confers resistance to paclitaxel treatment.…”

Section: P38 Enhancing Resistance To Targeted Therapies and Chemothermentioning

confidence: 99%

Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity

Lee

Rauch

Kölch

2020

IJMS

489

338

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Mitogen-activated protein kinase (MAPK) pathways represent ubiquitous signal transduction pathways that regulate all aspects of life and are frequently altered in disease. Here, we focus on the role of MAPK pathways in modulating drug sensitivity and resistance in cancer. We briefly discuss new findings in the extracellular signaling-regulated kinase (ERK) pathway, but mainly focus on the mechanisms how stress activated MAPK pathways, such as p38 MAPK and the Jun N-terminal kinases (JNK), impact the response of cancer cells to chemotherapies and targeted therapies. In this context, we also discuss the role of metabolic and epigenetic aberrations and new therapeutic opportunities arising from these changes.

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Down-regulation of miR-29b in carcinoma associated fibroblasts promotes cell growth and metastasis of breast cancer

Cited by 54 publications

References 36 publications

Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis

Sinomenine restrains breast cancer cells proliferation, migration and invasion via modulation of miR-29/PDCD-4 axis

Identification of Potential Therapeutic Targets Among CXC Chemokines in Breast Tumor Microenvironment Using Integrative Bioinformatics Analysis

Targeting MAPK Signaling in Cancer: Mechanisms of Drug Resistance and Sensitivity

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