Then, we explored the function of MALAT1-miR-145 in radiosensitivity of cervical cancers cells and demonstrated that si-MALAT1 and miR-145 had some level of synergic effect in reducing cancer cell colony formation, cell cycle regulation, and inducing apoptosis.
Although MALAT1 is highly evolutionary conserved in mammals and plays an important role in cancer and metastasis, MALAT1 is not essential for development in a knockout mouse model under normal physiological conditions.
In this study, we found that MALAT1 was downregulated in breast tumor cell lines and cancer tissue, and showed that knockdown of MALAT1 in breast cancer cell lines induced an epithelial-to-mesenchymal transition (EMT) program via phosphatidylinositide-3 kinase-AKT pathways.
However, lncRNA MALAT1 expression was not associated significantly with age (<45 vs. ≥ 45, P = 0.343), gender (female vs. male, P = 0.196), family history of cancer (yes vs. no, P = 0.665), and tumor location (supratentorial vs. infratentorial, P = 0.170).
By characterizing this sense/anti-sense pair we uncovered the complexity of MALAT1 locus regulation, describing new potential candidates for cancer targeting.
The lncRNA metastasis associated lung adenocarcinoma transcript 1 (Malat1) is overexpressed in many types of cancer, including hepatocarcinoma, and induces cell proliferation in several cell lines in vitro.
The results confirmed that the cancer prevention effects triggered by restored ABI3BP and depleted MALAT1 as evidenced by suppressed cell growth and enhanced cell senescence.
In this review, we first update on the role of MALAT1 in tumorigenesis and then discuss possible molecular mechanisms that underline the MALAT1-mediated gene regulation, leading to cancer invasion and metastasis.
The expression of MALAT1 was evaluated in cancer tissue and paired adjacent normal tissue samples from 77 middle thoracic ESCC patients who received radical surgical resection using QRT-PCR.
Importantly, subgroup analyses disclosed that increased MALAT1 expression had a poor OS among different cancer types (Estrogen-dependent cancer: pooled HR = 2.656, 95% CI 1.560-4.523; urological cancer: pooled HR = 1.952, 95% CI 1.189-3.204; glioma: pooled HR = 2.315, 95% CI 1.643-3.263; digestive cancer: pooled HR = 2.451, 95% CI 1.862-3.227).
A meta-analysis based on several gamma-retrovirus integration profiling (GRIP) studies in human cells (CD34+, K562, HepG2) revealed a similar cancer gene bias but also remarkable cell-type specificity, with prominent exceptions including a universal integration hotspot at the long non-coding RNA MALAT1.
Recent studies reveal that long non-coding RNAs (lncRNAs) have been shown to have important regulatory roles in cancer biology, and lncRNA MALAT-1 expression is upregulated in some tumors.
Tongue squamous cell carcinoma (TSCC) is the second most common malignancy in oral carcinoma. lncRNA metastasis-associated lung adenocarcinoma transcript 1 (<i>MALAT1</i>) was regarded as an oncogenic factor in various carcinomas.
Taken together, our data suggest that upregulation of MALAT1 was mediated by the transcription factor Sp1 in A549 lung cancer cells, and Sp1 could be therapeutic target for cancer.
Notably, different or opposite phenotypes resulting from different strategies for inactivating <i>MALAT1</i> have been observed, which led to distinct models for <i>MALAT1'</i>s functions and mechanisms of action in cancer and metastasis.
Collectively, our study demonstrates that cancer cell-specific chromatin-chromatin interactions are formed at the <i>MALAT1</i> locus under hypoxia, implicating a novel mechanism of MALAT1 regulation in cancer.