Targeting HER3 with miR-450b-3p suppresses breast cancer cells proliferation

Zhao, Zhenze; Li, Rui; Sha, Sha; Wang, Qiong; Mao, Weidong; Liu, Tao

doi:10.4161/cbt.29923

Cited by 35 publications

(26 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to being associated with aging, 8 Parkinsonʼs disease, and pulmonary hypertension, 13,14 miR-450b-3p has been reported to suppress breast cancer cell proliferation by targeting HER3. 10 Similarly, in this study, cell proliferation of HCC cell lines was found to be inhibited by miR-450b-3p overexpression in HCC either in vitro or in vivo. This inhibitory effect of miR-450b-3p on cell proliferation was also confirmed by cell-cycle assay and dephosphorylation of AKT signaling.…”

Section: Discussionsupporting

confidence: 70%

See 1 more Smart Citation

MicroRNA‐450b‐3p inhibits cell growth by targeting phosphoglycerate kinase 1 in hepatocellular carcinoma

Chen

Zhuang

Wang

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

Dysregulation of microRNAs frequently contributes to the occurrence and progression of human diseases, including hepatocellular carcinoma (HCC). In this study, the role of miR‐450b‐3p in HCC was investigated. Gene Expression Omnibus database and HCC specimens were used to evaluate the expression level of miR‐450b‐3p and the patient's prognosis. Cell functional analyses and tumor xenograft model were used to assess the role of miR‐450b‐3p in HCC. Bioinformatics was used to predict the downstream target gene of miR‐450b‐3p, which was verified by dual‐luciferase reporter assay. MiR‐450b‐3p was found to be downregulated in HCC cell lines and tissues, compared with nontransformed immortal hepatic cells and adjacent normal liver tissues, respectively. Lower expression of miR‐450b‐3p was associated with poor overall survival and disease‐free survival in patients with HCC. Ectopic expression of miR‐450b‐3p inhibited HCC cell viability, colony formation, and cell‐cycle progression in vitro, and suppressed the growth of HCC xenograft tumors in vivo. Interestingly, a negative correlation between miR‐450b‐3p and phosphoglycerate kinase 1 (PGK1) protein was observed among HCC specimens. Additionally, miR‐450b‐3p inhibited PGK1 expression and phosphorylation of protein kinase B in HCC cell lines. Further experiments confirmed that PGK1 was a direct target of miR‐450b‐3p. Moreover, restoration of PGK1 abrogated the inhibitory effect of miR‐450b‐3p on HCC proliferation and cell division. In conclusion, miR‐450b‐3p is downregulated in human HCC and exerts tumor suppressive effects at least in part by inhibiting PGK1.

show abstract

Section: Discussionsupporting

confidence: 70%

“…Previous research showed that miR-450b-3p could inhibit breast cancer proliferation by targeting the 3′UTR of human epidermal growth factor receptor 3 (HER3) mRNA. 10 Therefore, we hypothesized that miR-450b-3p may also contribute to the malignant progression of HCC.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA‐450b‐3p inhibits cell growth by targeting phosphoglycerate kinase 1 in hepatocellular carcinoma

Chen

Zhuang

Wang

et al. 2019

J of Cellular Biochemistry

View full text Add to dashboard Cite

show abstract

“…3). [60][61][62][63] As we describe below, 2 major lines of evidence motivated the current intensified interest in intercepting HER3 in human tumors: First, oncogenic mutant forms have recently been identified in approximately 10% of solid tumors and second, several studies indicated that HER3 plays pivotal roles in several compensatory processes that underlay emergence of resistance to certain cancer drugs. 64,65 …”

Section: Targeted Cancer Therapy Directed At the Egfr (Her/ Erbb) Familymentioning

confidence: 99%

“…63 Likewise, several antisense oligonucleotides or microRNAs seems able to downregulate HER3, such as a locked nucleic acid (LNA)-based HER3 antisense oligonucleotide called EZN-3920, 95 which improves the anti-tumor activity of TKIs, and miR-450b-3p, which inhibits proliferation of breast cancer cells. 60 Targeting mRNAs with LNA EZN-3920 provided promising preclinical strategy but further development remains a challenge. Another indirect strategy is the use of HSP90 inhibitors, such as tanespimycin (17-AAG).…”

Section: Others Indirect Strategiesmentioning

confidence: 99%

Emerging anti-cancer antibodies and combination therapies targeting HER3/ERBB3

Gaborit

Lindzen

Yarden

2015

Human Vaccines & Immunotherapeutics

View full text Add to dashboard Cite

Cancer progression depends on stepwise accumulation of oncogenic mutations and a select group of growth factors essential for tumor growth, metastasis and angiogenesis. Agents blocking the epidermal growth factor receptor (EGFR, also called HER1 and ERBB1) and the co-receptor called HER2/ERBB2 have been approved over the last decade as anti-cancer drugs. Because the catalytically defective member of the family, HER3/ERBB3, plays critical roles in emergence of resistance of carcinomas to various drugs, current efforts focus on antibodies and other anti-HER3/ERBB3 agents, which we review herein with an emphasis on drug combinations and some unique biochemical features of HER3/ERBB3.

show abstract

“…Studies have described that miRNAs are aberrantly expressed in human breast cancer and are involved in the proliferation, apoptosis, and cell cycle of breast cancer cells by modulating different molecules or signaling pathways. 7,8 In 2015, Sanjay et al 9 reported that miR-495 were downregulated in peripheral blood mononucleated cells of breast cancer. Wang et al 10 proved that upregulation of miR-495 could dramaticlly suppress the proliferation of breast cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Lnc RNA SNHG20 participated in proliferation, invasion, and migration of breast cancer cells via miR‐495

Guan

Zhang

Chen

et al. 2018

J of Cellular Biochemistry

View full text Add to dashboard Cite

To explore the mechanism of lnc SNHG20 in the regulation of proliferation, invasion, and migration of breast cancer cells. mRNA levels of SNHG20, miR-495, and HER2 were detected by qRT-PCR. Protein level of HER2 was measured by Western blot. Cell proliferation, invasion, and migration were detected by CCK-8 assay, Boyden chamber assay, and Transwell assay. The combination between SNHG20 and miR-495 was confirmed by RNA pull down assay. The combination between miR-495 and HER2 was confirmed by luciferase report assays. We also established breast cancer-bearing mice model and analyzed tumor volumes. Our data showed SNHG20 expression was significantly upregulated, miR-495 expression was significantly downregulated, and HER2 expression was significantly upregulated in breast cancer tissues and cell lines. Besides, SNHG20 promoted the proliferation, invasion, and migration of breast cancer cells. We also found SNHG20 negatively regulated miR-495, and miR-495 could negatively regulate HER2. Moreover, we discovered that SNHG20 regulated HER2 via miR-495. SNHG20 regulated proliferation, invasion, and migration of breast cancer cells via miR-495/HER2. Finally, we confirmed the mechanism of SNHG20 in the regulation of proliferation, invasion, and migration in breast cancer-bearing mice model. SNHG20 regulates HER2 via miR-495 to promote proliferation, invasion, and migration of breast cancer cells.

show abstract

Targeting HER3 with miR-450b-3p suppresses breast cancer cells proliferation

Cited by 35 publications

References 33 publications

MicroRNA‐450b‐3p inhibits cell growth by targeting phosphoglycerate kinase 1 in hepatocellular carcinoma

MicroRNA‐450b‐3p inhibits cell growth by targeting phosphoglycerate kinase 1 in hepatocellular carcinoma

Emerging anti-cancer antibodies and combination therapies targeting HER3/ERBB3

Lnc RNA SNHG20 participated in proliferation, invasion, and migration of breast cancer cells via miR‐495

Contact Info

Product

Resources

About