Heat shock factor 2 is associated with the occurrence of lung cancer by enhancing the expression of heat shock proteins

Zhong, Yi; Cheng, Hongzhong; Peng, Hao; Tang, Shicong; Wang, Ping

doi:10.3892/ol.2016.5368

Cited by 23 publications

(30 citation statements)

References 34 publications

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“…Increased expression of heat shock factor 2 has been reported in numerous types of cancers. HSF2 in lung cancer was up-regulated compared with the matched normal tissues [ 23 ]. The low expression of HSF2 was correlated with high Gleason score, metastasis, and poor survival of prostate cancer patients.…”

Section: Discussionmentioning

confidence: 99%

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ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

et al. 2018

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BackgroundPrevious research found that ALG3 is associated with cervical cancer, but the role of ALG3 in breast cancer was still unknown.Material/MethodsThe expression of ALG3 in breast carcinoma tissues was determined by immunochemistry. The ability of cellular proliferation, migration, and invasion was determined by CCK-8 assay, wound healing migration assay, and cell invasion assays, respectively. The binding between HSF2 and promoter of ALG3 was determined by ChIP assay.ResultsThere was an increased expression of ALG3 in breast cancer tissues compared to normal breast tissues (p<0.05). High expression of ALG3 was significantly correlated with poor OS (p<0.05). ALG3 expression was significantly increased in cancer samples with advanced stages (stage III/IV) compared with those in the early stages of disease (stage I/II) (p<0.05). The staining intensity of ALG3 was significantly correlated to the tumor grade (grades 2–3 versus 1, p<0.05). Silencing ALG3 or HSF2 inhibited the proliferation, migration, and invasion abilities of MCF-7 cells. Silencing ALG3 retarded the growth of MCF-7 cells in vivo.ConclusionsSilencing ALG3 inhibited MCF-7 cells growth in vitro and in vivo. HSF2 activated ALG3 and promoted the growth of breast carcinoma.

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Section: Discussionmentioning

confidence: 99%

“…The expression of HSF2 is significantly increased in lung cancer tissues. Overexpression of HSF2 promotes cell growth and cell migration [ 23 ]. The transcription of miR-183/-96/-182 is regulated by HSF2.…”

Section: Discussionmentioning

confidence: 99%

ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

et al. 2018

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“…Research has shown that there was a signi cant positive correlation between PM2.5 concentration and cancer mortality [29]. In ammation, particularly chronic in ammation, is strongly associated with the development of cancer [30]. ACCD may provide the prevention and treatment of in ammation through cancers-associated pathways in PM2.5induced lung in ammation.…”

Section: Discussionmentioning

confidence: 99%

Gene expression profiling to explore the protective effect of Antrodia cinnamomea compound decoction on PM2.5-induced lung inflammation in rats

Wang

Chen²,

Meng

et al. 2020

Preprint

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BackgroundAntrodia cinnamomea compound decoction (ACCD), a Chinese herbal extract composed of Antrodia cinnamomea, Rhinacanthus nasutus (L.) Kurz and Phellinus igniarius (L. ex Fr.), were widely used with anti-inflammatory activity. However, the effects and mechanisms of ACCD on the lung inflammation induced by PM2.5 are not fully understood. This study aims to reveal the effect of ACCD on PM2.5-induced lung inflammation and analyze the possible mechanisms through gene chip expression profiling. MethodsMale Wistar rats were subjected to lung damage by stimulation with 10% PM2.5, with/without ACCD (0.67g/kg/d) intervention. The HE, AB-PAS staining and IL-1β were performed to evaluate the effect of ACCD in the treatment of lung inflammation caused by PM2.5. In addition, the extracted lung genes were detected based on the gene chip expression profile. Bioinformatics analysis and quantitative real-time polymerase chain reaction assay (Q-PCR) were used to analysis and verify the related differentially expressed genes (DEGs). ResultsResults showed that instillation of PM2.5 increased the inflammatory cells immersion in the airways and the acid mucus content in the tracheal epithelium compared with the sham group, and it increased the IL-1β levels in Bronchoalveolar lavage fluid (BALF). ACCD reduced inflammatory cell immersion in airways, alleviated goblet cell metaplasia in tracheal epithelium and reduced IL-1β levels in BALF. A total of 99 genes with significant differential expression were identified (p < 0.05) after ACCD treatment compared with the model group, including 48 up-regulated and 51 down-regulated genes. Bioinformatics analysis showed that these DEGs were mainly related to inflammatory response and significantly enriched in cancer signaling pathway. Five of the DEGs were subjected to Q-PCR and three of them (Plcβ-1, Axin2, Ccbe1) were significant difference (p < 0.05). ConclusionOur study suggests that ACCD may exert anti-inflammatory effects on PM2.5-induced lung inflammation via the cancer pathway, and that Plcβ-1, Axin2, and Ccbe1 may be key targets of ACCD action on PM2.5-induced lung inflammation. This work could provide genomic clues for the continued study of ACCD for the therapy of PM2.5-induced lung inflammation.

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“…Inhibitors that target the proteasome or the N-terminus of Hsp90 induce the expression of HSF2 [17,18]. Increased expression of HSF2 is observed in lung cancer samples along with increased HSP levels [19]. Conversely, in prostate cancer, HSF2 suppresses tumor invasion by promoting acinar morphogenesis [20].…”

Section: Introductionmentioning

confidence: 99%

HSF1: Primary Factor in Molecular Chaperone Expression and a Major Contributor to Cancer Morbidity

Prince

Lang

Guerrero-Gimenez

et al. 2020

Cells

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Heat shock factor 1 (HSF1) is the primary component for initiation of the powerful heat shock response (HSR) in eukaryotes. The HSR is an evolutionarily conserved mechanism for responding to proteotoxic stress and involves the rapid expression of heat shock protein (HSP) molecular chaperones that promote cell viability by facilitating proteostasis. HSF1 activity is amplified in many tumor contexts in a manner that resembles a chronic state of stress, characterized by high levels of HSP gene expression as well as HSF1-mediated non-HSP gene regulation. HSF1 and its gene targets are essential for tumorigenesis across several experimental tumor models, and facilitate metastatic and resistant properties within cancer cells. Recent studies have suggested the significant potential of HSF1 as a therapeutic target and have motivated research efforts to understand the mechanisms of HSF1 regulation and develop methods for pharmacological intervention. We review what is currently known regarding the contribution of HSF1 activity to cancer pathology, its regulation and expression across human cancers, and strategies to target HSF1 for cancer therapy.

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Heat shock factor 2 is associated with the occurrence of lung cancer by enhancing the expression of heat shock proteins

Cited by 23 publications

References 34 publications

ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

ALG3 Is Activated by Heat Shock Factor 2 and Promotes Breast Cancer Growth

Gene expression profiling to explore the protective effect of Antrodia cinnamomea compound decoction on PM2.5-induced lung inflammation in rats

HSF1: Primary Factor in Molecular Chaperone Expression and a Major Contributor to Cancer Morbidity

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