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Founded Year

2013

Stage

IPO | IPO

Total Raised

$10M

Date of IPO

12/30/2014

About BBI Life Sciences

BBI Life Sciences (HKG:1035) provides life science research tools and services including molecular biology kits, biochemicals, synthetic genes, and synthetic oligos. It offers chemical and biological reagents, DNA synthesis, molecular biology kits, proteins, antibodies, and laboratory consumables. The company was founded in 2013 and is based in Shanghai, China.

Headquarters Location

698 XiangMin Road, SongJiang District

Shanghai, Shanghai,

China

+86) 21 800 820 1016

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Expert Collections containing BBI Life Sciences

Expert Collections are analyst-curated lists that highlight the companies you need to know in the most important technology spaces.

BBI Life Sciences is included in 1 Expert Collection, including Synthetic Biology.

S

Synthetic Biology

238 items

Companies involved in design and development of new biological parts, devices, and systems; as well as the re-design of existing biological systems.

Latest BBI Life Sciences News

Combined effects of naringin and doxorubicin on the JAK/STAT signaling pathway reduce the development and spread of breast cancer cells

Feb 3, 2024

Abstract Breast cancer therapy options are limited due to its late diagnosis and poor prognosis. Doxorubicin is the fundamental therapy approach for this disease. Because chemotherapy has numerous adverse effects, the scope of the existing research was to appraise the synergetic effect of doxorubicin and naringin and explore the underlying mechanism. The cytotoxicity of doxorubicin and naringin on MCF-7 was monitored. Furthermore, the expression of STAT3 and JAK1 as well as the apoptotic and metastatic related genes (Bax, Bcl-2, Survivin, and VEGF) were conducted by immunoblotting assay and qRT-PCR. In addition, a wound healing test was utilized to appraise the migration and metastasis of MCF-7. Our results revealed that naringin and doxorubicin had a synergetic inhibitory influence on MCF-7 cells growth and migration. The synergetic action of doxorubicin and naringin effectively hindered the expression of STAT3, JAK1, Bcl-2, Survivin, and VEGF, with a boost in the level of Bax compared to cells treated with either doxorubicin or naringin. In conclusion, our findings imply that combining doxorubicin with naringin may be a favorable strategy for inhibiting the growth of breast cancer. Introduction Breast cancer is the top frequent and the major prevalent reason of death among Egyptian women. Despite significant progress in many developing countries, Egypt's 5-year survival rate remained lower, between 28 and 68%, as a result of late diagnosis and a insufficiently prognosis 1 . Breast cancer treatment is often complicated and may be ineffective due to intrinsic or acquired drug resistance in cancer cells and severe side effects of chemotherapeutic agents 2 , 3 . One of the most popular anticancer medications is doxorubicin, which is used to treat both metastatic and early-stage breast cancer. Unfortunately, because of its oxidative stress action, its use is linked to the emergence of severe cumulative dose-related cardiotoxicity, myelosuppression, and treatment resistance 4 . As a result, it is preferable to combine it with other anticancer agents in order to lower its dosage without sacrificing its effectiveness 5 . Different research reported that high intake of vegetables and fruits may prevent cancer growth and decreased risk of different human cancers due to the presence of polyphenolic compounds, flavonoids 6 , 7 , 8 , 9 . Flavonoids are a big class of phenol-containing phytochemicals found in many fruits, vegetables, and some medicinal herbs that exert different biological functions involving antioxidant, anti-inflammatory, and anticancer 10 , 11 . Naringin (4′,5,7-Trihydroxyflavanone-7-rhamnoglucoside) is natural flavonoid found in grapefruit, orange, and Kino 12 , 13 . Previous investigations have revealed that naringin has numerous pharmacological impacts, such as anti-inflammatory, antioxidant, antimicrobial, and anti-carcinogenic activities 14 . Furthermore, it has the capability to reduce cell propagation and growth in various human malignancies like lung, melanoma, and breast by targeting several signal transduction pathways 15 , 16 . Li et al., exhibited that naringin reduced cell outgrowth and propped up apoptosis as well as blocked cell cycle at G0/G1phase in triple negative breast cancer by suppressing the pathway of β-catenin 17 . Zhou et al., suggested that naringin restrained the growth of thyroid cancer cells and encouraged the apoptosis by suppressing the path of phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) 18 . The signaling pathway of Janus kinase/signal transducers and activators of transcription (JAK/STAT) constitute an important signaling machinery which regulate many critical cellular activities such as proliferation, development, and differentiation, inflammation, apoptosis, and angiogenesis 19 . It has been previously informed that abnormal activation of STAT3 induce oncogenic processes in various cancers such as prostate, lung, ovary, leukemia, and breast 20 , 21 . Therefore, finding an inhibitor of STAT3 might be a promising approach in prevention and targeted therapy of cancer. Thus, this study was designated to investigate the antitumor activity of naringin alone or combined with doxorubicin against breast cancer through blockage of the JAK/STAT signaling route. Methods Cell culture Breast malignant cell line, MCF-7, and human skin fibroblast (HSF) from VACSERA, (the Egyptian Company for Production of Vaccines, Sera, and Drugs) were grown in RPMI-1640 medium with high glucose and L-glutamine content, 10% fetal bovine serum (FBS), and 1% streptomycin/penicillin (100 µg/ml streptomycin and 100 U/ml penicillin) (Sigma Aldrich Chemical Co., St. Louis, MO, USA). Cells were kept at 37 °C with 5% CO2. When confluent, they were passaged at 1:4 ratio. Cell viability assay The cytotoxic impact of naringin (98% purity, Solarbio, China) and doxorubicin (Sigma, USA) on the growth of MCF-7 cells was evaluated using the previously reported Sulforhodamine B (SRB) assay (Sigma-Aldrich Chemical Co., USA) 22 . In addition, the cytotoxic effect of naringin on HSF cells was evaluated. In a 96-well plate, MCF-7, and HSF cells (4.0 × 103 cells/well) were seeded. On the next day, MCF-7 cells were subjected to various dosages of naringin (NAR) (5, 10, 15, 20 and 25 μg/ml), doxorubicin (DOX) (1, 2, 4, 8, 16 and 32 μg/ml) for 48h. HSF cells were subjected to different NAR concentrations (5, 10, 15, 20, 25, 50, and 100 μg/ml). After treatments, cells were settled in 10% trichloroacetic acid for one hour at 4 °C. Finally, SRB 0.4% (w/v) was added for 30 min before washing with 1% acetic acid. SRB-bound cells have been dissolved down by a pH 10.5 solution of 10 mM Tris. Using a microplate reader, the absorbance was determined at 570 nm (TecanSunriseTM, Germany). Half-maximal inhibitory concentration (IC50) values, utilizing sigmoidal fitting equation, were calculated (GraphPad Prism program). Colony formation assay The antiproliferative effect of doxorubicin and naringin on MCF-7 cells were confirmed using clonogenicity assay. In 6-well plate, 1 × 103 MCF-7 cells were plated and treated for 48h with 1/2 IC50 DOX, IC50 NAR and their combination. The media was then replaced with fresh media and the cells were allowed to grow and proliferate for 10 days at 37 °C. After that, the colonies were fixed with methanol and stained with 0.5% crystal violet. The colonies of 50 cells were imaged and counted using inverted microscope 23 . Quantitative real-time polymerase chain reaction (qRT-PCR) 500,000 MCF-7 cells were planted in 25 mm flasks. After overnight incubation, cells were given 1/2 IC50 DOX, IC50 NAR and a combination (Comb) of 1/2 IC50 DOX and IC50 NAR for 48h. Using the miRNeasy Mini Kit (Qiagen, Germany), total RNA was purified from treated and untreated cells in accordance with the Qiagen company's guidelines. A NanoDrop-2000 spectrophotometer (ThermoFisher Scientific, USA) was used to measure the amount of RNA. Utilizing the Quantitect RNA reverse transcription kit (Qiagen, Germany) in accordance with the manufacturer's guidelines, complementary DNA (cDNA) was synthesized from 1 µg of RNA. qPCR was used to determine the relative expression levels of STAT3, JAK1, Bcl-2 associated x protein (Bax), B-cell lymphoma 2 (Bcl-2), Survivin, vascular endothelial growth factor (VEGF), matrix metalloproteinases (MMP-2, MMP-9) using a quantinova SYBR Green reagent kit from Qiagen with cDNA as the template. As an internal control for mRNAs, glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used. We bought primer assays from Qiagen in Germany. On the ViiA™ 7 PCR machine (Applied Biosystems, USA), all the qPCR reactions were run in triplicate. Data were analysed using the ΔΔCt comparative approach and the fold of change = 2−ΔΔCt 24 . The primers used in this work are ready made (Cat No. 249900, Qiagen, Germany). JAK1(GeneGlobe ID-QT00050225), STAT3 (GeneGlobe ID-QT00068754), Bax (GeneGlobe ID-QT00031192), Bcl-2 (GeneGlobe ID-QT00025011), Survivin (GeneGlobe ID-QT01679664), VEGF (GeneGlobe ID-QT01682072), MMP-2 (GeneGlobe ID-QT00088396), and MMP-9 (GeneGlobe ID-QT00040040). Western blot analysis Naringin and doxorubicin-treated cells were assessed by western blot analysis for STAT3, p-STAT3, JAK1, p-JAK1, Bax, Bcl-2, Survivin, and VEGF proteins in whole-cell extracts as previously described 25 . The cells were lysed in an ice-cold lysis solution that contained the following ingredients: 50 mM Tris–HCl pH 7.4, 150 mM NaCl, 1% Nonidet P-40, 1 mM ethylenediaminetetraacetic acid (EDTA), and 1X Protease Inhibitor Cocktail to create the cell extracts. Using the Bradford Protein Assay Kit (SK3041) (Bio Basic Inc, Ontario, Canada), the protein concentration in each sample was calculated according to manufacturer's guidelines. After electrophoresis, the proteins were electrotransferred to a polyvinylidene fluoride (PVDF) membrane, blocked for 1 h at room temperature with 3% bovine serum albumin, then probed with a variety of primary antibodies (Table 1 ) overnight at 4 °C. The membrane was then washed, kept for 1 h at room temperature with a horseradish peroxidase (HRP)-conjugated secondary antibody solution, and lastly analyzed using an enhanced chemiluminescence (ECL) reagent. Original images (in supplementary file) were captured using UVITEC digital imaging system which typically produces highly contrast bands. These bands were then quantified by its software package (UK) and the densities of each band were normalized to β-actin. Table 1 Antibodies used in western blot analysis.

BBI Life Sciences Frequently Asked Questions (FAQ)

  • When was BBI Life Sciences founded?

    BBI Life Sciences was founded in 2013.

  • Where is BBI Life Sciences's headquarters?

    BBI Life Sciences's headquarters is located at 698 XiangMin Road, SongJiang District, Shanghai.

  • What is BBI Life Sciences's latest funding round?

    BBI Life Sciences's latest funding round is IPO.

  • How much did BBI Life Sciences raise?

    BBI Life Sciences raised a total of $10M.

  • Who are the investors of BBI Life Sciences?

    Investors of BBI Life Sciences include Qiming Venture Partners.

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