[Progranulin (PGRN) promotes invasion and migration of mouse breast cancer 4T1 cells by promoting epithelial-mesenchymal transition of cancer cells and activating ERK1/2 pathway].

Objective To investigate the effect of progranulin (PGRN) on the invasion and migration of mouse breast cancer 4T1 cells and its mechanism. Methods After treated with PGRN (1 μg/mL) for 24 hours, the invasion ability of breast cancer 4T1 cells was detected by Transwell invasion assay, the migration ability was detected by scratch test, and the epithelial cadherin (E-cadherin), vimentin mRNA expression was detected by real-time fluorescent quantitative PCR. Western blot assay was used to detect the expression of E-cadherin, vimentin, extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphorylated ERK1/2 (p-ERK1/2).

Honokiol inhibits the growth of SKBR3 cells.

Background: Breast cancer is one of the most malignant tumors in the reproductive system and has a poor prognosis. Finding drugs with high efficiency, low side-effects, and low cost has become a research hotspot.

Methods: In the present study, we treated SK-BR-3 cells with different doses of honokiol.

PGRN TAMs-derived exosomes inhibit breast cancer cell invasion and migration and its mechanism exploration.

Unlabelled: Breast cancer is one of the most malignant diseases world-wide and ranks the first among female cancers. Progranulin (PGRN) plays a carcinogenic role in breast cancer, but its mechanisms are not clear. In addition, there are few reports on the relationship between PGRN and tumor-associated macrophages (TAMs).

Nucleus-located PDK1 regulates growth, invasion and migration of breast cancer cells.

Aims: It is well known that pyruvate dehydrogenase kinase 1 (PDK1) is highly expressed in breast cancer (BC) tissues and promotes tumor growth, but the underlying mechanisms of this process are unclear. Here, we investigated the effects of nuclear PDK1 on growth, migration and invasion in human BC cells.

Main Methods: The sub-cellular localization of PDK1 in BC cells was performed with subcellular fractionation followed by Western blot and immunofluorescence.

[Molecular mechanism of macrophages derived from PGRN gene knockout mice inhibit invasion and migration of breast cancer cells].

Objective To explore the functions and mechanisms of macrophages derived from PGRN gene knockout (PGRN ) C57BL/6 mice in the invasion and migration of breast cancer cells. Methods Breast cancer cells were cultured in conditioned medium of macrophages derived from WT and PGRN mice. Transwell assay and scratch assay were used to detect the invasion and migration ability of cancer cells.

Fiber optic surface plasmon resonance biosensor for detection of PDGF-BB in serum based on self-assembled aptamer and antifouling peptide monolayer.

Herein, a home-build fiber optic surface plasmon resonance (FO-SPR) biosensing platform has been developed for highly sensitive detection of platelet-derived growth factor (PDGF-BB) based aptamer-functionalized AuNPs for signal enhancement. In this biosensor, the PDGF-BB aptamer was used to specifically capture PDGF-BB, and the antifouling peptide demonstrated great ability for resisting non-specific adsorption. After a sandwich reaction, the aptamer, PDGF-BB and aptamer-functionalized AuNPs complexes were formed on the fiber optic (FO) probe surface to significantly amplify FO-SPR signal.

The miR-186-3p/EREG axis orchestrates tamoxifen resistance and aerobic glycolysis in breast cancer cells.

Tamoxifen resistance is one of the major challenges for its medical uses in estrogen receptor (ER)-positive breast cancer. Aerobic glycolysis, an anomalous characteristic of glucose metabolism in cancer cells, has been shown to associate with the resistance to chemotherapeutic agents. It remains, however, largely unclear whether and how tamoxifen resistance contributes to aerobic glycolysis in breast cancer.