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Effects of the Long Non-Coding RNA HOST2 On the Proliferation, Migration, Invasion and Apoptosis of Human
Background/Aims:
This study aimed to explore the effects of the long non-coding RNA HOST2 (lnc-HOST2) on the proliferation, migration, invasion and apoptosis of osteosarcoma cells.
Methods:
Osteosarcoma tissues and adjacent normal tissues from 52 patients were selected. Human osteosarcoma cell lines (SaOS2, HOS, U2OS and MG-63) were collected and cultured; MG-63 cells had the highest lnc-HOST2 expression and thus were used in subsequent experiments. Then, MG-63 cells were transfected and divided into the blank (no transfection), si-CON (transfected with negative control siRNA) and si-lnc-HOST2 (transfected with small interference lnc-HOST2 siRNA) groups. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the expression of lnc-HOST2 in primary tissues and cells. Cell growth was detected using the CCK-8 and colony formation assays. Cell doubling time was detected. Cell migration and invasion were observed using the scratch test and Transwell assays. Cell apoptosis and cell cycle progression of osteosarcoma cells were detected using flow cytometry with annexin V/PI double staining and PI staining, respectively.
Results:
The level of lnc-HOST2 expression in the si-lnc-HOST2 group was significantly decreased compared to that in the blank and si-CON groups. The OD values in the si-lnc-HOST2 group were significantly lower than those in the blank and si-CON groups. Compared to the blank and si-CON groups, the si-lnc-HOST2 group presented significant decreases in the colony number and healing rates after scratching. The number of invasive cells in the si-lnc-HOST2 group was significantly less than that in the blank and si-CON groups. In the si-lnc-HOST2 group, the cell cycle was mainly halted in the G1 phase, and the apoptosis rate and doubling time in this group were significantly higher than those in the blank group and si-CON group.
Conclusions:
Inhibition of lnc-HOST2 could suppress the proliferation, migration, and invasion and promote the apoptosis of osteosarcoma cells.
Insights
Inhibition of long non-coding RNA HOST2 (lnc-HOST2) suppresses osteosarcoma cell growth, migration, and invasion. This study demonstrates that targeting lnc-HOST2 promotes apoptosis in osteosarcoma cells, offering a potential therapeutic strategy.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Osteosarcoma is a primary bone malignancy with limited treatment options.
- Long non-coding RNAs (lncRNAs) play crucial roles in cancer development and progression.
- The specific role of lnc-HOST2 in osteosarcoma remains largely unexplored.
Purpose of the Study:
- To investigate the functional role of lnc-HOST2 in osteosarcoma.
- To determine the effects of lnc-HOST2 on osteosarcoma cell proliferation, migration, invasion, and apoptosis.
Main Methods:
- Analysis of lnc-HOST2 expression in osteosarcoma tissues and cell lines.
- Manipulation of lnc-HOST2 expression using small interfering RNA (siRNA) in MG-63 cells.
- Assessment of cell proliferation, migration, invasion, apoptosis, and cell cycle using CCK-8, colony formation, scratch, Transwell, and flow cytometry assays.
Main Results:
- lnc-HOST2 expression was significantly reduced in the si-lnc-HOST2 group.
- Inhibition of lnc-HOST2 suppressed cell proliferation, colony formation, migration, and invasion.
- lnc-HOST2 inhibition led to G1 phase cell cycle arrest and increased apoptosis rates.
Conclusions:
- lnc-HOST2 acts as a pro-tumorigenic factor in osteosarcoma.
- Inhibiting lnc-HOST2 effectively suppresses osteosarcoma cell growth and metastasis.
- Targeting lnc-HOST2 presents a promising therapeutic strategy for osteosarcoma treatment.
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