Related Experiment Video
Updated: Aug 22, 2025
Author Spotlight: Unveiling the Role of TMOD3 in Platinum Resistance and Immune Infiltration in Ovarian Cancer
Published on: August 2, 2024
LncRNA MEG3 promotes cisplatin sensitivity of cervical cancer cells by regulating the miR-21/PTEN axis
Ying Du1, Gang Geng2, Chunquan Zhao1
1Department of Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, China.
Background:
Cervical cancer (CC) is a common gynecological malignancy worldwide. Some patients perform serious resistance after chemotherapy, and long-stranded non-coding RNA MEG3 is reported to be involved in the regulation of chemoresistance in many solid tumors. However, its involvement in cervical adenocarcinoma has not been reported.
Methods:
Hela cell lines, cisplatin-resistant cell lines (Hela-CR) and nude mice were used in this study. After MEG3 was overexpressed or knocked down in cells by the lentivirus vector, cell growth was detected by the CCK-8 assay, and cell migration was evaluated using Transwell assay. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to examine the expression of MEG3, miR-21 and PTEN mRNA. Apoptosis was detected by flow cytometry. The targeting relationship between mRNAs was predicted and verified using dual-luciferase reporter gene experiments. Western blot was executed to examine Bax, cleaved-caspase 3, Bcl-2, PTEN and GAPDH expression. Cells were injected into the mice to form xenograft tumors to compare tumorigenesis capacity.
Results:
We demonstrated that MEG3 was down-regulated in cervical cancer by analyzing the TCGA database. Moreover, knockdown of MEG3 promoted CC cell proliferation, migration and inhibited the apoptosis. These changes of CC cells were more pronounced under cisplatin treatment. Further studies showed that the MEG3/miR-21/PTEN axis affected cisplatin sensitivity in cervical cancer cells, and these results of recue assay were used to confirm this conclusion.
Conclusions:
MEG3 performing as ceRNA promotes cisplatin sensitivity in CC cells through the miR-21/PTEN axis.
Insights
Long-stranded non-coding RNA MEG3 enhances cisplatin sensitivity in cervical cancer cells by regulating the miR-21/PTEN axis. This finding offers a potential therapeutic target for overcoming chemoresistance in cervical adenocarcinoma.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Cervical cancer (CC) is a prevalent gynecological malignancy globally.
- Chemotherapy resistance is a significant challenge in CC treatment.
- The role of long-stranded non-coding RNA MEG3 in cervical adenocarcinoma chemoresistance remains unelucidated.
Purpose of the Study:
- To investigate the role of MEG3 in cervical cancer chemoresistance.
- To elucidate the underlying molecular mechanism involving the MEG3/miR-21/PTEN axis.
Main Methods:
- Analysis of TCGA database for MEG3 expression in CC.
- Overexpression and knockdown of MEG3 in Hela cells using lentivirus vectors.
- Assays for cell proliferation (CCK-8), migration (Transwell), apoptosis (flow cytometry), and protein expression (Western blot).
- Dual-luciferase reporter assays to confirm targeting relationships.
- In vivo studies using xenograft tumor models in nude mice.
Main Results:
- MEG3 was found to be downregulated in cervical cancer.
- MEG3 knockdown promoted CC cell proliferation and migration while inhibiting apoptosis.
- These effects were exacerbated under cisplatin treatment.
- The MEG3/miR-21/PTEN axis was identified as a key regulator of cisplatin sensitivity in CC cells.
Conclusions:
- MEG3 functions as a competing endogenous RNA (ceRNA).
- MEG3 promotes cisplatin sensitivity in cervical cancer cells.
- The therapeutic effect is mediated through the miR-21/PTEN axis.
Related Concept Videos
02:39lncRNA - Long Non-coding RNAs
01:22MicroRNAs
02:23Abnormal Proliferation
01:06Induced Pluripotent Stem Cells
Somatic...
02:57Targeted Cancer Therapies
There are several types of targeted therapies against...