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Updated: Feb 17, 2026

Monitoring Hippo Signaling Pathway Activity Using a Luciferase-based Large Tumor Suppressor LATS Biosensor
Published on: September 13, 2018
Study on mechanism about long noncoding RNA MALAT1 affecting pancreatic cancer by regulating Hippo-YAP signaling
Yongping Zhou1, Ting Shan2, Wenzhou Ding1
1Department of Hepatobiliary, Wuxi Second Hospital, Nanjing Medical University, Wuxi, Jiangsu, China.
Abstract:
By investigating the migration and invasion ability in pancreatic cancer, this study probed into the lncRNA MALAT1 molecular mechanism on Hippo-YAP signaling. The expression of lncRNA MALAT1 in PC tissues and cells was detected by qRT-PCR and Western blot. The effect of si-MALAT1 on proliferation was determined by CCK-8 assay. Cell apoptosis, migration, and invasion were respectively detected by flow cytometry assay, wound healing assay, and transwell assay. Western blot and immunohistochemistry were successively used for detecting LATS1 and YAP1 expression in pancreatic cancer tissues. The microarray analysis determined that lncRNA MALAT1 in pancreatic cancer was highly expressed. LncRNA MALAT1 presented an extremely high expression level in pancreatic cancer tissues and cells. After transfected with si-MALAT1, the proliferation of AsPC-1 cells decreased, induce apoptosis of AsPC-1 cells, and migration and invasion ability were reduced. The tendency of LATS1 expression level was down-regulated and YAP1 show the opposite trend in the Hippo-YAP signaling. The in vivo assay was found that the tumor to be small in size and volume, and the expression of Ki-67 was decreased. High expression of lncRNA MALAT1 in PC disorder the proliferation, apoptosis, and migration and invasion ability via influence Hippo-YAP signaling pathway.
Insights
High expression of long non-coding RNA MALAT1 in pancreatic cancer (PC) promotes tumor growth and metastasis by inhibiting the Hippo-YAP signaling pathway. Silencing MALAT1 reduces proliferation and invasion, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Pancreatic cancer (PC) is a highly aggressive malignancy with poor prognosis.
- Long non-coding RNAs (lncRNAs) play critical roles in cancer development and progression.
- The Hippo-YAP signaling pathway is frequently dysregulated in various cancers, including PC.
Purpose of the Study:
- To investigate the molecular mechanism of lncRNA MALAT1 in pancreatic cancer.
- To explore the role of lncRNA MALAT1 in regulating the Hippo-YAP signaling pathway.
- To assess the impact of lncRNA MALAT1 on cancer cell proliferation, apoptosis, migration, and invasion.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and Western blot to detect MALAT1, LATS1, and YAP1 expression.
- Cell Counting Kit-8 (CCK-8) assay for proliferation.
- Flow cytometry for apoptosis.
- Wound healing and Transwell assays for migration and invasion.
- Immunohistochemistry and in vivo tumor xenograft models.
Main Results:
- lncRNA MALAT1 was highly expressed in PC tissues and cells.
- Silencing MALAT1 (si-MALAT1) decreased proliferation, induced apoptosis, and reduced migration and invasion of PC cells (AsPC-1).
- MALAT1 dysregulated LATS1 (down-regulated) and YAP1 (up-regulated) expression within the Hippo-YAP pathway, leading to increased tumor growth and Ki-67 expression in vivo.
Conclusions:
- High expression of lncRNA MALAT1 in pancreatic cancer promotes tumor progression.
- lncRNA MALAT1 influences proliferation, apoptosis, migration, and invasion by modulating the Hippo-YAP signaling pathway.
- lncRNA MALAT1 represents a potential therapeutic target for pancreatic cancer treatment.
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