Knockdown of Sal‐like 4 expression by siRNA induces apoptosis in colorectal cancer

Hesari, AmirReza; Rajab, Shadi; Rezaei, Marzieh; Basam, Maryam; Golmohamadi, Sara; Ghasemi, Faezeh

doi:10.1002/jcb.28433

Cited by 6 publications

(6 citation statements)

References 69 publications

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“…Overexpression of antiapoptotic Bcl-2 inhibits cell apoptosis and leads to an imbalance between enhanced proliferation and weakened programmed death through downregulation of Bax [73,74]. SALL4 overexpression in MDS and AML cells results in an increase in Bcl-2 expression and cell survival [75], whereas SALL4 knockdown markedly inhibits Bcl-2 expression in prostate cancer [76], breast cancer [16,77], colorectal cancer (CRC) [78], and nasopharyngeal carcinoma (NPC) [79], and it induces the expression of pro-apoptotic Bax in prostate cancer [76] and NPC [79].…”

Section: Sall4 Regulates Expression Of Bcl-2 and Baxmentioning

confidence: 99%

SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

Sun

et al. 2022

IJMS

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SALL4, a member of the SALL family, is an embryonic stem cell regulator involved in self-renewal and pluripotency. Recently, SALL4 overexpression was found in malignant cancers, including lung cancer, hepatocellular carcinoma, breast cancer, gastric cancer, colorectal cancer, osteosarcoma, acute myeloid leukemia, ovarian cancer, and glioma. This review updates recent advances of our knowledge of the biology of SALL4 with a focus on its mechanisms and regulatory functions in tumors and human hematopoiesis. SALL4 overexpression promotes proliferation, development, invasion, and migration in cancers through activation of the Wnt/β-catenin, PI3K/AKT, and Notch signaling pathways; expression of mitochondrial oxidative phosphorylation genes; and inhibition of the expression of the Bcl-2 family, caspase-related proteins, and death receptors. Additionally, SALL4 regulates tumor progression correlated with the immune microenvironment involved in the TNF family and gene expression through epigenetic mechanisms, consequently affecting hematopoiesis. Therefore, SALL4 plays a critical oncogenic role in gene transcription and tumor growth. However, there are still some scientific hypotheses to be tested regarding whether SALL4 is a therapeutic target, such as different tumor microenvironments and drug resistance. Thus, an in-depth understanding and study of the functions and mechanisms of SALL4 in cancer may help develop novel strategies for cancer therapy.

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Section: Sall4 Regulates Expression Of Bcl-2 and Baxmentioning

confidence: 99%

SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

Sun

et al. 2022

IJMS

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“…Colorectal cancer (CRC) is the main cause of cancer‐related death worldwide. The incidence has kept rising in recent years.…”

Section: Mir‐124 and Colorectal Cancermentioning

confidence: 99%

MicroRNA‐124: An emerging therapeutic target in cancer

et al. 2019

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MicroRNAs (miRNAs) are noncoding single‐stranded RNAs, approximately 20‐24 nucleotides in length, known as powerful posttranscriptional regulators. miRNAs play important regulatory roles in cellular processes by changing messenger RNA expression and are widely involved in human diseases, including tumors. It has been reported in the literature that miRNAs have a precise role in cell proliferation, programmed cell death, differentiation, and expression of coding genes. MicroRNA‐124 (miR‐124) has reduced exparession in various human neoplasms and is believed to be related to the occurrence, development, and prognosis of malignant tumors. In our review, we focus on the specific molecular functions of miR‐124 and the downstream gene targets in major cancers, which provide preclinical evidence for the treatment of human cancer. Although some obstacles exist, miR‐124 is still attracting intensive research focus as a promising and effective anticancer weapon.

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“…The silenced SALL4 gene expression is associated with the inhibition of proliferation via cell cycle arrest at the G1/early S phase and apoptosis by decreasing the protein expression of Bcl‐2 in breast, colorectal, lung, and gastric cancer 15,44–49 . knockdown of SALL4 inhibits the proliferation of MCF‐7/ADR cells by arresting the cell cycle in the G1 phase, accompanied by a significant reduction of cyclin D1 and CDK4 expression 50 .…”

Section: The Oncogenic Roles Of Sall4 In Cancermentioning

confidence: 99%

The new advance of SALL4 in cancer: Function, regulation, and implication

Abouelnazar

Zhang

Wang

et al. 2023

Clinical Laboratory Analysis

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SALL4 (split-like protein 4) is a member of the mammalian homologs of the Drosophila homoeotic gene spalt (sal) and acts as a zinc finger transcription factor to govern the self-renewal and pluripotency of embryonic stem cells. SALL4 expression gradually decreases during development and is even absent in most adult tissues. However, increasing evidence suggests that SALL4 expression is restored in human cancers and its aberrant expression is associated with the progression of many hematopoietic malignancies and solid tumors. The potent roles of SALL4 in regulating cancer cell proliferation, apoptosis, metastasis, and drug resistance have been reported. SALL4 plays a dual role in epigenetic modulation by acting as either an activator or a repressor of its target genes. Furthermore, SALL4 interacts with other partners to control the expression of many downstream genes and the activation of various key signaling transduction pathways. SALL4 is considered as a promising diagnostic and prognostic biomarker and therapeutic target for cancer. In this review, we highlighted the major advances in the roles and mechanisms of SALL4 in cancer and the therapeutic strategies for targeting SALL4 to treat cancer.

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Knockdown of Sal‐like 4 expression by siRNA induces apoptosis in colorectal cancer

Cited by 6 publications

References 69 publications

SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

SALL4 Oncogenic Function in Cancers: Mechanisms and Therapeutic Relevance

MicroRNA‐124: An emerging therapeutic target in cancer

The new advance of SALL4 in cancer: Function, regulation, and implication

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