CKS1B promotes the progression of hepatocellular carcinoma by activating JAK/STAT3 signal pathway

Liu, Xitao; Zhao, De-Fang

doi:10.1080/19768354.2021.1953142

Cited by 7 publications

(7 citation statements)

References 25 publications

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“…Moreover, flow cytometry revealed a higher rate of apoptosis ovarian cancer cells that had been treated with si-CKS1B; moreover, the levels of Bax and cleaved caspase 3 were higher. Similarly, Liu et al [16] reported that the silencing of CKS1B markedly suppressed the survival and viability of hepatocellular carcinoma cells, thus suppressing the development and metastasis of hepatocellular carcinoma. In lung adenocarcinoma, CKS1B serves as a vital regulator involved in promoting the proliferation of tumors [17].…”

Section: Discussionmentioning

confidence: 87%

CKS1B promotes the growth of ovarian cancer cells by regulating the expression of PD-L1

2023

EJGO

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Ovarian cancer has high rates of morbidity and mortality and a poor prognosis. A growing body of research suggests that CDC28 protein kinase regulatory subunit 1B (CKS1B) influences the progression of numerous carcinomas. However, the specific mechanism of CKS1B in ovarian cancer has yet to be elucidated. Here, this study aimed to investigate the involvement of CKS1B in the progression of ovarian cancer. Initially, we collected data from the Cancer Genome Atlas (TCGA) website and ovarian cancer tissues showed elevated CKS1B expression compared to healthy tissues, indicating a poorer prognosis. Immunohistochemistry (IHC) was used to detect CKS1B and programmed cell death 1-ligand 1 (PD-L1) levels and demonstrated that CKS1B is positively related to PD-L1 expression. Then, short-interfering (si)-CKS1B or sinegative control (si-NC) constructs were transfected into SKOV3 and OVCAR3 cells. Subsequently, cell viability was measured by cell counting kit-8 (CCK8) and colony formation assays, and the extent of apoptosis was assessed using flow cytometry. We found that CKS1B silencing inhibited cell growth and promoted cell apoptosis in ovarian cancer. In addition, the expression levels of CKS1B, B-cell lymphoma-2 (BCL2)associated X (Bax), cleaved-caspase3 and PD-L1 were determined by western blotting. Furthermore, to investigate whether the inhibitory effects of si-CKS1B on ovarian cancer is related to the levels of PD-L1, we added PD-L1 to si-CKS1B transfected cells and found that cells that had been supplemented with PD-L1 exhibited an increased cell growth rate and a reduced apoptosis rate than si-CKS1B cells. Collectively, our data we demonstrated high levels of CKS1B in ovarian cancer cells, and found that the knockdown of CKS1B could alleviate the development of ovarian tumors by dysregulating the level of PD-L1 expression.

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Section: Discussionmentioning

confidence: 87%

CKS1B promotes the growth of ovarian cancer cells by regulating the expression of PD-L1

2023

EJGO

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“…In depth study implied that the loss of EPN3 might suppress NSCLC cell malignant phenotype via inactivating the JAK1/2‐STAT3 pathway. As we known, the aberrantly activation of the JAK/STAT3 pathway is involved in the malignant development of multiple cancers, such as hepatocellular carcinoma, pancreatic cancer, gastric cancer as well as breast cancer, and so on 41–44 . Similarly, several literatures have confirmed that the activation of the JAK/STAT3 pathway promotes the malignant development of NSCLC 45–47 .…”

Section: Discussionmentioning

confidence: 88%

“…As we known, the aberrantly activation of the JAK/STAT3 pathway is involved in the malignant development of multiple cancers, such as hepatocellular carcinoma, pancreatic cancer, gastric cancer as well as breast cancer, and so on. [41][42][43][44] Similarly, several literatures have confirmed that the activation of the JAK/STAT3 pathway promotes the malignant development of NSCLC. [45][46][47] The treatment targeting the JAK/STAT3 pathway has been proposed to be a promising regimen for tumors.…”

Section: Loss Of Epn3 Might Suppress the In Vivo Growth Of Nsclc Cell...mentioning

confidence: 87%

EPN3 plays oncogenic role in non‐small cell lung cancer by activating the JAK1/2‐STAT3 pathway

Meng

Zhang

Zhu

et al. 2023

Environmental Toxicology

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The effect of Epsin 3 (EPN3) on non‐small cell lung cancer (NSCLC) has not yet been clearly elucidated. This study identified the exact function of EPN3 on NSCLC progression. EPN3 expression in NSCLC patients were analyzed based on the Cancer Genome Atlas database. Kaplan–Meier analysis was implemented to research the effect of EPN3 on patients' survival. EPN3 expression in clinical tissues of 62 NSCLC cases was monitored by real‐time quantitative reverse transcription polymerase chain reaction, immunohistochemistry and Western blot. A549 and H1299 cells were transfected with EPN3 shRNA and treated by RO8191 (20 μM). Proliferation was researched by cell counting kit‐8 and 5‐ethnyl‐2 deoxyuridine assays. Apoptosis was monitored by flow cytometry. Migration and invasion was assessed by Transwell experiment. EPN3 effect on A549 cell in vivo growth was researched using nude mice. RO8191 (200 μg) was intratumoral injected into mice. Immunohistochemistry and Western blot was implemented to monitor protein expression in cells and xenograft tumor tissues. EPN3 was abnormally up‐regulated in NSCLC patients and cells, indicating a lower overall survival. Loss of EPN3 weakened proliferation, migration and invasion, induced apoptosis, and repressed epithelial‐mesenchymal transition in NSCLC cells. Loss of EPN3 inactivated the JAK1/2‐STAT3 pathway in NSCLC cells. RO8191 treatment reversed the inhibition of EPN3 knockdown on the malignant phenotype of NSCLC cells. RO8191 intratumoral injection reversed the suppression of EPN3 silencing on NSCLC cell in vivo growth. EPN3 acted as an oncogene in NSCLC via activating the JAK1/2‐STAT3 pathway. EPN3 may be a promising target for NSCLC treatment.

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“…Low expression of Receptor coactivator 3 (NCOA3) may lead to decreased differentiation potential of embryonic stem cells in vitro and in vivo [ 24 ]. CKS1B regulates cell cycle processes by engaging with cyclin-dependent kinase (CDK) and SCF complex to affect cell proliferation [ 25 ]. MDM2, an E3 ubiquitin ligase, plays a crucial role in the differentiation of various cell types, including osteoblasts and myoblasts [ 26 ].…”

Section: Resultsmentioning

confidence: 99%

MIWE: detecting the critical states of complex biological systems by the mutual information weighted entropy

Xie,

Peng,

2024

BMC Bioinformatics

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Complex biological systems often undergo sudden qualitative changes during their dynamic evolution. These critical transitions are typically characterized by a catastrophic progression of the system. Identifying the critical point is critical to uncovering the underlying mechanisms of complex biological systems. However, the system may exhibit minimal changes in its state until the critical point is reached, and in the face of high throughput and strong noise data, traditional biomarkers may not be effective in distinguishing the critical state. In this study, we propose a novel approach, mutual information weighted entropy (MIWE), which uses mutual information between genes to build networks and identifies critical states by quantifying molecular dynamic differences at each stage through weighted differential entropy. The method is applied to one numerical simulation dataset and four real datasets, including bulk and single-cell expression datasets. The critical states of the system can be recognized and the robustness of MIWE method is verified by numerical simulation under the influence of different noises. Moreover, we identify two key transcription factors (TFs), CREB1 and CREB3, that regulate downstream signaling genes to coordinate cell fate commitment. The dark genes in the single-cell expression datasets are mined to reveal the potential pathway regulation mechanism.

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CKS1B promotes the progression of hepatocellular carcinoma by activating JAK/STAT3 signal pathway

Cited by 7 publications

References 25 publications

CKS1B promotes the growth of ovarian cancer cells by regulating the expression of PD-L1

CKS1B promotes the growth of ovarian cancer cells by regulating the expression of PD-L1

EPN3 plays oncogenic role in non‐small cell lung cancer by activating the JAK1/2‐STAT3 pathway

MIWE: detecting the critical states of complex biological systems by the mutual information weighted entropy

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