Dataset Information

Proteomic Analysis of LncPTEN1 RNA Pulldown in Lung Cancer Cells Using LC-MS/MS

ABSTRACT: This study aims to identify the molecular function of LncPTEN1 in lung cancer and explore its associated proteins and pathways. Using RNA pulldown coupled with mass spectrometry, we investigated the protein interactions of LncPTEN1 in A549 lung cancer cells. The experiment included three biological replicates with samples 1, 2, 3 as control group and samples 4, 5, 6 as LncPTEN1 overexpression group. The study revealed potential binding partners including Vimentin and Trim16, providing insights into the regulatory mechanisms of LncPTEN1 in lung cancer metastasis.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Zichu Shen

LAB HEAD: Zichu Shen

PROVIDER: PXD057469 | Pride | 2025-06-23

REPOSITORIES: Pride

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Publications

LncPTEN1, a long non-coding RNA generated from PTEN, suppresses lung cancer metastasis through the regulation of EMT progress.

Shen Zichu Z Zhong Ailin A Zhang Chun C Tang Xiaowei X Zhao Xuyang X Hou Zhiyuan Z Liang Hui H Yin Yuxin Y

Non-coding RNA research 20250524

Lung cancer is among the most frequently observed and lethal malignancies globally, and metastasis represents a critical determinant of patient outcomes. PTEN, a well-established tumor suppressor, has emerged as an important regulator in lung cancer progression. However, the molecular mechanism of PTEN gene suppressing lung cancer metastasis lacks deeper exploration. In this research, we identify and characterize LncPTEN1, a novel long non-coding RNA generated from PTEN gene. We sh ...[more]

PMID: 40521243

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Project description:K-RAS activating mutations occur frequently in non-small cell lung cancer (NSCLC), leading to aberrant activation of Ras-MAPK signaling pathway that contributes to the malignant phenotype. However, the development of Ras-targeted therapeutics remains challenging. Here, we show that MED23, a component of the multisubunit Mediator complex that is known to integrate signaling and gene activities, is selectively important for Ras-active lung cancer. By screening a large panel of human lung cancer cell lines with or without a Ras mutation, we found that Med23 RNAi specifically inhibits the proliferation and tumorigenicity of lung cancer cells with hyperactive Ras activity. Med23-deficiency in fibroblasts selectively inhibited the oncogenic transformation induced by Ras but not by c-Myc. Transcription factor ELK1, which is phosphorylated by MAPK for relaying the Ras signaling to MED23, was also required for the Ras-driven oncogenesis. Transcriptiome analysis revealed that MED23 and ELK1 co-regulate a common set of target genes enriched in regulating cell cycle and proliferation to support the Ras-dependency. Furthermore, correlated with the strength of Ras signaling as indicated by the ELK1 phosphorylation level, MED23 was up-regulated by Ras-transformation, and was found to be overexpressed in both Ras-mutated lung cancer cell lines and primary tumor samples. Remarkably, lower Med23 expression predicts better survival in Ras-active lung cancer patients and xenograft mice. Collectively, our findings demonstrate a critical role for MED23 in enabling the 'Ras-addiction' of lung carcinogenesis, thus providing a vulnerable target for the treatment of Ras-active lung cancer. To gain a genome-wide understanding of how MED23 and ELK1 control gene expression in Ras-active lung cancer cells, we performed gene profiling experiments to analyze the transcriptomes from control, si-Med23, or si-Elk1 A549 cells. The si-Ctrl, si-Med23 and si-Elk1 A549 cells were cultured in the normal condition. Then the cells were harvested for RNA extraction and hybridization on Affymetrix microarrays. The analysis contain 9 samples. si-Ctrl cells have three replicates (si-Ctrl#1, si-Ctrl#2 and si-Ctrl#3), and the si-Med23 or si-Elk1 group contains three different cell lines that harbor three different RNAi oligos against Med23 or Elk1 (si-Med23A, B, C and si-Elk1A, B, C).

Project description:Minichromosome maintenance protein 2 (MCM2) is a licensing factor for DNA replication. It interacts with other MCM proteins to comprise MCM2-7 complex, which acts as a helicase for DNA unwinding and limits DNA replication to one round per cell cycle. MCM2 has been widely used as a biomarker for proliferation in many types of cancer. However, the molecular regulation underlying MCM2 in lung cancer cells is poorly understood. In this study, we investigated the role of MCM2 in lung adenocarcinoma A549 (wild-type p53) and H1299 (null p53) cells. MCM2 overexpression increased cell proliferation in A549 cells while silencing MCM2 decreased cell proliferation in H1299 cells. We performed global quantitative phosphoproteomic analysis to uncover the important downstream networks regulated by MCM2 in lung cancer cells. We identified 1484 phosphorylation sites in 593 phosphoproteins of MCM2-overexpressed A549 cells. Of these phosphosites, 110 phosphoproteins were significantly changed in response to MCM2 overexpression. In addition, we identified 1599 phosphorylation sites in 592 phosphoproteins of MCM2-silenced H1299 cells. Of these phosphosites, 57 phosphoproteins were significantly changed in response to MCM2 silencing. The differentially regulated phosphoproteins are involved in biological functions such as RNA splicing, cell cycle and cytoskeleton regulation. Functional study demonstrated that MCM2 overexpression promoted cell migration in A549 cells. Moreover, silencing MCM2 inhibits cell migration and induces cell cycle arrest in H1299 cells. Furthermore, we observed a common phosphorylation change at Ser-99 of high mobility group protein HMG-I/HMG-Y (HMGA1) in both MCM2 overexpression and silencing, indicating an important regulatory effect of Ser-99 HMGA1 on lung cancer cells. The phosphoproteomic profiling of MCM2 in lung cancer cells provides new insight about phosphorylation networks regulated by MCM2 and reveals novel targets for lung cancer therapy.

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Dataset Information

Proteomic Analysis of LncPTEN1 RNA Pulldown in Lung Cancer Cells Using LC-MS/MS

Dataset's files

Publications

LncPTEN1, a long non-coding RNA generated from <i>PTEN</i>, suppresses lung cancer metastasis through the regulation of EMT progress.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

Proteomic Analysis of LncPTEN1 RNA Pulldown in Lung Cancer Cells Using LC-MS/MS

Dataset's files

Publications

LncPTEN1, a long non-coding RNA generated from &lt;i&gt;PTEN&lt;/i&gt;, suppresses lung cancer metastasis through the regulation of EMT progress.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets

LncPTEN1, a long non-coding RNA generated from <i>PTEN</i>, suppresses lung cancer metastasis through the regulation of EMT progress.