Upregulation of SALL4 by EGFR activation regulates the stemness of CD44-positive lung cancer

Du, Wenjing; Ni, Lan; Liu, Baojun; Wei, Ying; Lv, Yubao; Qiang, Sujing; Dong, Jingcheng; Liu, Xijun

doi:10.1038/s41389-018-0045-7

Cited by 32 publications

(33 citation statements)

References 40 publications

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“…Prior studies have shown that high expression of SALL4 is closely related to tumorigenesis and development [ 27 , 28 , 29 , 30 , 31 ]. Yang et al reported that the reduction of SALL4 markedly diminishes the tumorigenicity of leukemic cells [ 27 ].…”

Section: Discussionmentioning

confidence: 99%

“…Yang et al reported that the reduction of SALL4 markedly diminishes the tumorigenicity of leukemic cells [ 27 ]. SALL4 has also been shown to promote the migration, invasion, and metastasis of lung cancer cells [ 28 ]. Pan et al discovered that SALL4 activates long noncoding RNA DANCR in gastric cancer cells, and exerts its oncogenic activities through the activation of the β-catenin pathway [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

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miR-103/miR-195/miR-15b Regulate SALL4 and Inhibit Proliferation and Migration in Glioma

et al. 2018

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Glioma is the common highly malignant primary brain tumor. However, the molecular pathways that result in the pathogenesis of glioma remain elusive. In this study, we found that microRNA-103 (miR-103), microRNA-195 (miR-195), or microRNA-15b (miR-15b), which all have the same 5′ “seed” miRNA portion and share common binding sites in the SALL4 3′-untranslated region (UTR), were downregulated in glioma tissues and cell lines. These miRNAs suppressed glioma cell proliferation, migration, and invasion, induced cell apoptosis, and decreased the level of the SALL4 protein, but not that of SALL4 mRNA, which was identified as a direct target of all three miRNAs. The caspase-3/7 activity expression in U251 cells overexpressing these miRNAs was rescued during SALL4 upregulation. An obvious inverse correlation was observed between SALL4 and miR-103 or miR-195 expression levels in clinical glioma samples. Moreover, enforced expression of SALL4 stimulated cell proliferation, migration, and invasion. In conclusion, these data suggest that miR-103, miR-195, and miR-15b post-transcriptionally downregulated the expression of SALL4 and suppressed glioma cell growth, migration, and invasion, and increased cell apoptosis. These results provide a potential therapeutic target that may downregulate SALL4 in glioma.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

miR-103/miR-195/miR-15b Regulate SALL4 and Inhibit Proliferation and Migration in Glioma

et al. 2018

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“…Pathways enriched in dLUAD are shown in green, molecular regulatory network as ESCs (35,36). Similarly, lung cancer cells also show a higher expression of ESC-associated genes (12,(37)(38)(39). Validating this observation, we proved that LUADs share a much higher transcriptomic (including lncRNAs expression) overlap with ESCs compared to NL cells ( Figure 1A).…”

Section: Discussionmentioning

confidence: 52%

A Greedy Algorithm-Based Stem Cell LncRNA Signature Identifies a Novel Subgroup of Lung Adenocarcinoma Patients With Poor Prognosis

et al. 2020

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Cancer stem cells play an essential role in therapy response and aggressiveness of various cancers, including lung adenocarcinoma (LUAD). Interestingly it also shares many features of embryonic stem cells (ESCs). Recently, long non-coding RNAs (lncRNAs) have emerged as a critical regulator of cell physiology. Here, we used expression data of ESCs, LUAD, and normal lung to identify 198 long non-coding hESC-associated lncRNAs (hESC-lncRNAs). Intriguingly, K-means clustering of hESC-associated lncRNAs identified a subgroup of LUAD patients [undifferentiated LUAD (uLUAD)] with high stem cell-like characteristic, decreased differentiation genes expression, and poor survival. We also observed that the uLUAD patients had overexpression of proteins associated with cell proliferation. Interestingly, uLUAD patients were highly enriched with the stemness-related gene sets, and had higher mutation load. A notable result observed was high infiltration of T cells and a higher level of neopeptides in uLUAD patients, making these patients an optimal candidate for immunotherapy. Further, feature selection using greedy algorithm identified 17-hESC-lncRNAs signature, which showed significant consistency with 198 hESC-lncRNAs-based classification, and identified a group of patients with high stem cell-like characteristic in the 10 most common cancer types and CCLE cell lines. These results suggest the conventional role of hESC-lncRNAs in stem cell biology. In summary, we identified a novel subgroup of LUAD patients (uLUAD) using a set of hESC-lncRNAs. The uLUAD patients had high stem cell-like characteristic and reduced survival rate and may be referred for immunotherapy. Furthermore, our analysis also showed the importance of lncRNAs in cancer and cancer stem cells.

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“…SALL4 abrogated the inhibitory effect of miR-3622a-3p on cancer stemness features of CRC cells SALL4 is believed to promote stemness features in many types of cancers 16,34,35 .…”

Section: Mir-3622a-3p Acted As a Tumor Suppressor By Targeting Sall4mentioning

confidence: 98%

MiR-3622a-3p acts as a tumor suppressor in colorectal cancer by reducing stemness features and EMT through targeting spalt-like transcription factor 4

et al. 2020

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MicroRNAs are a class of small non-coding RNAs which act as oncogenes or tumor suppressors through targeting specific mRNAs. Colorectal cancer (CRC) is one of the most common malignancies worldwide. MiR-3622a-3p is found to be decreased in colorectal cancer (CRC) by analyzing data from TCGA database and there are few reports about the role of miR-3622a-3p in cancers. Our research aimed to explore the effects of miR-3622a-3p on CRC. MiR-3622a-3p was found to be down-regulated in CRC tissues and cells by qRT-PCR. The effect of miR-3622a-3p on proliferation, apoptosis, cell cycle, migration and invasion of CRC cells were investigated by a serious of biological function assays and the results revealed that miR-3622a-3p could inhibit the malignant biological properties of CRC. We performed dual luciferase assay, RNA immunoprecipitation (RIP) assay and pull-down assay to confirm the interaction between miR-3622a-3p and spalt-like transcription factor 4 (SALL4). Western blot was carried out to determine the effects of miR-3622a-3p and SALL4 on stemness features and EMT. We found that miR-3622a-3p suppressed stemness features and EMT of CRC cells by SALL4 mRNA degradation. MiR-3622a-3p could inhibit CRC cell proliferation and metastasis in vivo with tumor xenograft model and in vivo metastasis model. The CRC organoid model was constructed with fresh CRC tissues and the growth of organoids was suppressed by miR-3622a-3p. Taken together, the results of our study indicate miR-3622a-3p exerts antioncogenic role in CRC by downregulation of SALL4. The research on miR-3622a-3p might provide a new insight into treatment of CRC.

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Upregulation of SALL4 by EGFR activation regulates the stemness of CD44-positive lung cancer

Cited by 32 publications

References 40 publications

miR-103/miR-195/miR-15b Regulate SALL4 and Inhibit Proliferation and Migration in Glioma

miR-103/miR-195/miR-15b Regulate SALL4 and Inhibit Proliferation and Migration in Glioma

A Greedy Algorithm-Based Stem Cell LncRNA Signature Identifies a Novel Subgroup of Lung Adenocarcinoma Patients With Poor Prognosis

MiR-3622a-3p acts as a tumor suppressor in colorectal cancer by reducing stemness features and EMT through targeting spalt-like transcription factor 4

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