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Multi-photon Imaging of Tumor Cell Invasion in an Orthotopic Mouse Model of Oral Squamous Cell Carcinoma
Published on: July 25, 2011
Alkannin restrains oral squamous carcinoma cell growth, migration and invasion by regulating microRNA-9/RECK axis
Yulong Mao1, Weiwei Zhang2, Ronghe Zhang2
1a Department of Oral and Maxillofacial Surgery, Binzhou Medical University Hospital , Binzhou , China.
Abstract:
Alkannin (ALK) has anti-inflammatory and anti-tumour activities. We tried to probe the underlying functions of ALK in oral squamous carcinoma (OSCC) cells growth, migration and invasion. OSCC cells viability was investigated after treatment with ALK. Then, BrdU, flow cytometry, Western blot and Transwell assays were executed to appraise proliferation, apoptosis, migration and invasion in OSCC cells with ALK stimulation. The biological functions of miR-9 were explored after miR-9 mimic/inhibitor transfection. The relevance of RECK and miR-9 was predicated by dual luciferase activity assay. JAK1/STAT3 and PI3K/AKT pathways were estimated by Western blot. Tumour formation in vivo was executed by xenograft tumours assay. We found that ALK restrained cell proliferation, facilitated apoptosis, repressed migration and invasion also interdicted JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells. miR-9 expression was upgraded in OSCC tissues but decreased in OSCC cells along with ALK administration; meanwhile, overexpressed miR-9 inverted the influences of ALK in OSCC cells growth, migration and invasion. RECK was predicated as a novel target gene of miR-9, and overexpressed RECK hindered JAK1/STAT3 and PI3K/AKT pathways in OSCC cells. ALK prohibited tumour formation in vivo. In conclusion, ALK restrained OSCC cells growth, migration and invasion via adjusting miR-9/RECK axis. Highlights ALK restrains cell growth, migration and invasion in OSCC cells; miR-9 is enhanced in OSCC tissues but is repressed by ALK in OSCC cells; miR-9 inverts the repressive effect of ALK on CAL-27 and SCC-9 cells; RECK is a novel target of miR-9; ALK or RECK hinders JAK1/STAT3 and PI3K/AKT pathways in CAL-27 and SCC-9 cells; ALK prohibits tumour formation in vivo.
Insights
Alkannin (ALK) inhibits oral squamous cell carcinoma (OSCC) growth, migration, and invasion by regulating the miR-9/RECK pathway. This natural compound also suppresses tumor formation in vivo, offering potential therapeutic strategies for OSCC.
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Oral squamous cell carcinoma (OSCC) is a prevalent malignancy with significant morbidity and mortality.
- Alkannin (ALK), a natural compound, exhibits anti-inflammatory and anti-tumor properties.
- Understanding ALK's mechanisms in OSCC is crucial for developing novel therapeutic interventions.
Purpose of the Study:
- To investigate the functional role of Alkannin (ALK) in regulating the growth, migration, and invasion of oral squamous cell carcinoma (OSCC) cells.
- To elucidate the molecular pathways and key regulatory elements, including miR-9 and RECK, involved in ALK's anti-cancer effects.
- To evaluate the therapeutic potential of ALK in an in vivo model of OSCC.
Main Methods:
- Cell viability, proliferation (BrdU), apoptosis (flow cytometry), migration, and invasion (Transwell assays) were assessed in OSCC cells treated with ALK.
- miR-9 mimic/inhibitor transfections were used to explore miR-9 functions.
- Dual luciferase activity assay identified RECK as a miR-9 target gene.
- Western blot analyzed JAK1/STAT3 and PI3K/AKT pathway activation.
- In vivo tumor formation was evaluated using xenograft assays.
Main Results:
- Alkannin (ALK) significantly inhibited OSCC cell proliferation, migration, and invasion while promoting apoptosis.
- ALK treatment led to decreased expression of miR-9 in OSCC cells, and conversely, miR-9 overexpression reversed ALK's inhibitory effects.
- RECK was identified as a direct target of miR-9, and its overexpression also suppressed OSCC cell aggressiveness.
- ALK and RECK were found to inhibit the JAK1/STAT3 and PI3K/AKT signaling pathways.
- ALK administration suppressed tumor growth in vivo.
Conclusions:
- Alkannin (ALK) exerts anti-cancer effects in oral squamous cell carcinoma (OSCC) by inhibiting cell growth, migration, and invasion.
- The mechanism involves the modulation of the miR-9/RECK axis, leading to the suppression of JAK1/STAT3 and PI3K/AKT signaling pathways.
- ALK demonstrates significant potential as a therapeutic agent for OSCC treatment, warranting further investigation.
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