The effects of Lycorine on PANC-1 cells.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1111805 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR29037809_1.fastq.gz | Fastqsanger.gz | |||
| SRR29037809_2.fastq.gz | Fastqsanger.gz | |||
| SRR29037812_1.fastq.gz | Fastqsanger.gz | |||
| SRR29037812_2.fastq.gz | Fastqsanger.gz |
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Project description:Lycorine (LY) is a natural alkaloid extracted from the Amaryllidaceae plant, it has been evaluated for its anticancer effects on pancreatic cancer cells and xenograft models. Our research presents a multi-faceted investigation of LY, including assessments of its impact on cell viability, proliferation, migration, invasion, and potential mechanisms of action.
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Project description:Ovarian cancer remains the most lethal gynecological malignancy worldwide, with poor prognosis due to chemotherapy resistance and cancer stem cell-driven recurrence. This study comprehensively investigates the antitumor effects of lycorine, a natural alkaloid derived from Lycoris radiata, on human ovarian cancer models. Our results demonstrate that lycorine significantly inhibits ovarian cancer cell proliferation, induces apoptosis, and suppresses cancer stemness properties through modulation of the PI3K/AKT signaling pathway. In vitro, lycorine treatment reduced the expression of stemness markers (CD133, CD44, NANOG, SOX2, OCT4, and LIN28) and impaired tumor sphere formation. RNA sequencing and pathway enrichment analysis confirmed significant inhibition of PI3K/AKT signaling, accompanied by decreased phosphorylation of AKT and mTOR. In vivo, lycorine (5 mg/kg) effectively suppressed tumor growth in A2780-luc xenograft models, reduced stem cell subpopulations, and exhibited minimal toxicity. Furthermore, lycorine sensitized ovarian cancer cells to cisplatin and counteracted cisplatin-induced enrichment of cancer stem cells. These findings highlight lycorine as a promising multi-target therapeutic agent against ovarian cancer, particularly for addressing stemness-driven chemoresistance and recurrence.
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Project description:Cholestatic liver disease (CLD) is characterized by the dysfunction of bile synthesis and excretion, leading to progressive liver injury or fibrosis, but lacks effective treatment drugs. Lycorine, an alkaloid isolated from Lycoris bulbs, possesses antiviral, anti-inflammatory, analgesic, cardioprotective activities. However, there has been no report concerning its effects on CLD so far. We evaluated the hepatoprotective effect of lycorine on intrahepatic cholestasis mouse models induced by α-naphthylisothiocyanate (ANIT) or after multidrug resistance protein 2 knockout (Mdr2-/-). RNA-Sequencing (RNA-Seq), cellular thermal shift assay (CETSA) and mass spectrometry analysis were used to investigate the regulated molecular mechanism of lycorine. Lycorine alleviated intrahepatic cholestasis by decreasing the expression of activating transcription factor 3 (ATF3), and inhibiting the nuclear accumulation of unphosphorylated ATF3, a transcription repression factor of the bile salt export pump (BSEP) responsible for bile acid (BA) secretion. Additionally, lycorine bound with transketolase (TKT) protein directly and promoted its ubiquitination degradation, disrupting the interaction between TKT and ATF3, resulting in the increased interaction between Rho-associated protein kinase 1(ROCK1) and ATF3 and subsequently BSEP transcription repression. Conclusively, our results shed light on the protective effects and mechanisms of lycorine against CLD, which pave way for the design of novel clinical therapeutic strategies.
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Project description:Gemcitabine has been a first-line therapeutic agent for pancreatic ductal adenocarcinoma (PDAC) pancreatic cancer; however, acquisition of resistance to gemcitabine remains a major challenge. We analyzed miRNAs expression profiles by array-based miRNAs analysis between gemcitabine–resistant (PANC-1/GEM) and parental PANC-1 cells.
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Project description:Background: Tyrosine kinase inhibitor (TKI) resistance is a significant factor exacerbating the burden on chronic myeloid leukemia (CML) patients and impacting clinical efficacy. The main goal is to offer new insights into overcoming drug resistance in treating CML. Methods: (IM) resistant K562/IM cells were generated using gradient induction. Responses to IM, lycorine, and autophagy modulators were assessed using CCK-8. Protein expression of Beclin-1, Atg5, LC3, Caspase-3, P62, Bax, Bcl-2, and P-gp was detected using Western blot. Lycorine-induced apoptosis and cell cycle changes were evaluated through flow cytometry, while autophagy alterations were detected using Monodansylcadaverine(MDC) staining. In the K562/IM mice model, Non-obese diabetic severe combined immunodeficent(NOD-SCID) mice were subcutaneously inoculated with K562/IM cells. After 17 days of lycorine injection, assessments included tumor size, Hematoxylin-eosin(HE) staining, and Ki67 expression. Results: After 72 hours of IM treatment, K562/IM cells showed a 55.86-fold increase in drug resistance compared to K562 cells. Lycorine treatment for 24 hours inhibited cell proliferation and induced G0/G1 phase cell cycle arrest and apoptosis in both K562 and K562/IM cells. MDC staining indicated reduced autophagy in K562/IM cells, mitigated by lycorine. In vivo experiments demonstrated reduced tumor size and Ki67 proliferation index in the lycorine treatment group (K562+L, K562/IM+L) compared to the control group, particularly in the drug-resistant group. However, no significant change in Ki67 was observed in the K562 group after lycorine treatment. Conclusion: In summary, K562/IM cells displayed heightened autophagy levels compared to K562 cells. Lycorine effectively impeded the proliferation of K562/IM cells through diverse mechanisms, including reduced autophagy, enhanced apoptosis, and induced cell cycle arrest.
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Project description:The zebrafish is a powerful model for the study of hematopoietic stem and progenitor cells (HSPC). We have developed a novel HSPC-specific transgenic line (Runx1+23:GFP). We have used this line in time-lapse live imaging studies to track the migration of HSPC during development. We have also performed a chemical genetic screen to find small molecules that modulate HSPC numbers during development. Treating embryos from 2-3 days post fertilization (2-3 dpf) then fixing for in situ staining with HSPC probes cmyb and runx1, we found the compound lycorine increased HSPC numbers. Applying this compound during time-lapse live imaging showed increased accumulation of Runx+ HSPC in the caudal hematopoietic tissue (CHT). Treatment from 2-3 dpf, then washing off the compound, had a sustained effect on the size of the HSPC with Runx+ numbers higher at 5 and 7 dpf. We have performed microarray analysis to elucidate the molecular changes within HSPC and endothelial cells after Lycorine treatment. We treated Runx1+23:GFP;kdrl:DsRed2 embryos from 2-3 dpf with 75 uM lycorine in 1% DMSO. We then dissociated the embryos and sorted the Runx+ GFP cells, the kdrl+ DsRed2 cells, and the non-fluorescent negative cells from the total embryo as a comparator population. Total RNA was amplified and biotin labled for hybridization on Affymetrix microarrays. 18 samples were collected and analyzed. There are 3 biological replicates. There are 3 cell type populations: 1) Runx+ HSPC; 2) kdrl+ endothelial cells; 3) non-fluorescent negative cells. There are cell populations from dissociated Lycorine-treated embryo pools, and control DMSO-treated embryo pools.
2015-01-15 | E-GEOD-56015 | biostudies-arrayexpress
Project description:High-throughput sequencing was performed to analyze gene expression profiles of RBE cells after the the inhibition of SQLE or FDFT1 by lentiviruses-mediated shRNA, or RBE cells treated with lycorine hydrochloride.
2023-08-18 | GSE240746 | GEO
Project description:Analysis of differentially expressing genes in whole genome wide analysis of ALPPL2 expressing Panc-1 cells (Panc-1+ve) via siRNA mediated knockdown of ALPPL2 Panc-1 +ve and Panc-1-ve cell lines were generated from Panc-1 cell line based upon its hetergenous binding to aptamer SQ2. Detailed procedure of generation of these cell lines are described in Pooja Dua, Hye Suk Kang, Seung-Mo Hong, Ming-Sound Tsao, Soyoun Kim, and Dong-ki Lee. 2012 Alkaline Phosphatase ALPPL2 is a novel pancreatic carcinoma-associated protein. Cancer Research A four chip study using total RNA recovered from Panc-1+ve cells transfected with siALPPL2-2, siALPPL2-3, siGFP control and Lipofectamine 2000 treatament . Each chip measures 45,033 genes with three 60 mer probe pairs per target.
2012-11-21 | E-GEOD-42427 | biostudies-arrayexpress
Project description:Analysis of differentially expressing genes in whole genome wide analysis of ALPPL2 expressing Panc-1 cells (Panc-1+ve) via siRNA mediated knockdown of ALPPL2 Panc-1 +ve and Panc-1-ve cell lines were generated from Panc-1 cell line based upon its hetergenous binding to aptamer SQ2. Detailed procedure of generation of these cell lines are described in Pooja Dua, Hye Suk Kang, Seung-Mo Hong, Ming-Sound Tsao, Soyoun Kim, and Dong-ki Lee. 2012 Alkaline Phosphatase ALPPL2 is a novel pancreatic carcinoma-associated protein. Cancer Research
2012-11-21 | GSE42427 | GEO