HSDL2 Acts as a Promoter in Pancreatic Cancer by Regulating Cell Proliferation and Lipid Metabolism

Han, Anna; Xu, Ran; Liu, Ying; Yin, Xianglin; Lin, Zhenhua; Yang, Wenge

doi:10.2147/ott.s287722

Cited by 9 publications

(14 citation statements)

References 31 publications

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“… 32 Hydroxysteroid dehydrogenase like protein 2 (Hsdl2), a member of the steroid dehydrogenase family, is located in peroxisomes and mitochondria, and can not only bind to peroxisomes, but also interact with the coenzyme NADPH, which plays an important role in fatty acid metabolism. 33 Research on these two proteins has focused on finding that their levels are significantly elevated in various cancers and can be used as markers for cancer diagnosis and as therapeutic targets. 34 , 35 Our study showed that Hsd17b4 and Hsdl2 were up-regulated in the heart and aorta.…”

Section: Discussionmentioning

confidence: 99%

Effects of High-Fat Diet on Cardiovascular Protein Expression in Mice Based on Proteomics

Pan¹,

Zhang²,

Ban³

et al. 2023

DMSO

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Purpose To investigate the effect of high-fat diet on protein expression in mouse heart and aorta using proteomic techniques. Methods A high-fat diet was used to construct an obese mouse model, and body weight was checked regularly. After the experiment, serum lipid and oxidative stress levels were measured. Proteomic detection of cardiac and aortic protein expression. Cardiac and aortic common differentially expressed proteins (Co-DEPs) were screened based on proteomic results. Subsequently, functional enrichment analysis and screening of key proteins were performed. Results A high-fat diet significantly increased body weight in mice. Obese mice had considerably higher levels of TC, TG, LDL-C, ROS, and MDA. In the heart and aorta, 17 Co-DEPs were discovered. The results of functional analysis of these proteins indicated that they were mainly related to lipid metabolism. Ech1, Decr1, Hsd17b4, Hsdl2 and Acadvl were screened as key proteins. In mice, a high-fat diet causes lipid metabolism to become disrupted, resulting in higher levels of oxidative stress and lipid peroxidation products. Conclusion Ech1, Decr1, Hsd17b4, Hsdl2 and Acadvl as cardiac and aortic Co-DEPs are closely related to lipid metabolism and may serve as potential diagnostic and therapeutic targets for obesity-induced cardiovascular disease.

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Section: Discussionmentioning

confidence: 99%

Effects of High-Fat Diet on Cardiovascular Protein Expression in Mice Based on Proteomics

Pan¹,

Zhang²,

Ban³

et al. 2023

DMSO

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“…HSDL2 was in highly expressed in human ovarian cancer and was positively correlated with tumor progression and lymphatic metastasis, meanwhile, HSDL2 knockdown inhibited tumorigenesis in vivo or vitro [ 20 ]. HSDL2 was highly expressed in pancreatic cancer and connected with shorter overall survival, meanwhile proliferation and lipid metabolism were further inhibited when HSDL2 was silenced in pancreatic cancer cell [ 14 ]. In this study, we detected the expression of HSDL2 in patients with CC.…”

Section: Discussionmentioning

confidence: 99%

“…Hydroxysteroid dehydrogenases like 2 (HSDL2) locates in 9q32, includes 12 exons and ubiquitously expresses in fat, liver and other tissues. Numerous studies had shown that the HSDL2 was a key factor of fatty acid regulatory in lipid metabolism [14] and abnormal HSDL2 expression was associated with a variety of cancers, such as bladder cancer [15], breast cancer [16], lung adenocarcinoma [17], thyroid carcinoma [18], cholangiocarcinoma [19], ovarian cancer [20], gliomas [21], pancreatic cancer [14] et al A large number of studies had shown that abnormal lipid metabolism could accelerate/decelerate the progression of CC [22]. HSDL2 regulated lipid metabolism, and abnormal expression of HSDL2 could promote the malignant characteristics of tumors [14,[23][24][25], including CC [23].…”

Section: Introductionmentioning

confidence: 99%

“…Numerous studies had shown that the HSDL2 was a key factor of fatty acid regulatory in lipid metabolism [14] and abnormal HSDL2 expression was associated with a variety of cancers, such as bladder cancer [15], breast cancer [16], lung adenocarcinoma [17], thyroid carcinoma [18], cholangiocarcinoma [19], ovarian cancer [20], gliomas [21], pancreatic cancer [14] et al A large number of studies had shown that abnormal lipid metabolism could accelerate/decelerate the progression of CC [22]. HSDL2 regulated lipid metabolism, and abnormal expression of HSDL2 could promote the malignant characteristics of tumors [14,[23][24][25], including CC [23]. Meanwhile, it was confirmed that miR-26a-5p was closely related to the progression of CC [26], but its specific molecular regulation mechanism is unclear.…”

Section: Introductionmentioning

confidence: 99%

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MiR-26a-5p regulates proliferation, apoptosis, migration and invasion via inhibiting hydroxysteroid dehydrogenase like-2 in cervical cancer cell

Xiao

Liu

et al. 2022

BMC Cancer

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Background Evidences have indicated that miR-26a-5p regulates the malignant properties of various tumor cells. However, the influences of miR-26a-5p on proliferation, apoptosis and invasion are still vague in the cervical cancer (CC) cells. Methods The miRNA microarray and real-time quantitative PCR (RT-qPCR) analysis were utilized to detect the expression of miR-26a-5p in the patients with CC. Kaplan–Meier plotter was performed to evaluate the overall survival (OS) of the patients with CC. The CCK-8, flow cytometry, transwell and wound healing analyses were respectively used to analyze proliferation, migration and invasion in the CC cells. RT-qPCR, western blot and IHC analysis were executed to measure the expression of hydroxysteroid dehydrogenase like-2 (HSDL2) in the patients with CC. Bioinformatics and luciferase reporter assay were carried out to verify the relationship of miR-26a-5p and HSDL2. Results The expression of miR-26a-5p was downregulated and low expression of miR-26a-5p indicated a poor OS in patients with CC. Overexpression of miR-26a-5p significantly inhibited proliferation, migration and invasion, accelerated apoptosis in the Hela and C33A cells. The expression of HSDL2 was upregulated, and negatively correlated with miR-26a-5p in the patients with CC. HSDL2 was directly targeted by miR-26a-5p and rescue experiments displayed that HSDL2 partially abolished proliferation, apoptosis, migration, and invasion induced by miR-26a-5p in CC cells. Conclusions MiR-26a-5p alleviated progression of CC by suppressing proliferation, migration and invasion, promoting apoptosis through downregulating HSDL2.

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“…Hydroxysteroid dehydrogenase-like (HSDL) 2 is a member of the short-chain dehydrogenase/reductase (SDR) superfamily that can catalyse the oxidation and reduction of various substrates, such as steroids, sugars, retinoids and fatty acids [ 7 ]. Previous studies have shown that HSDL2 is involved in lipid metabolism and the synthesis of cholesterol [ 8 , 9 ], displaying significant protumour function by promoting cell proliferation and inhibiting apoptosis [ 10 , 11 ], and has been reported to be associated with some cancers, such as pancreatic cancer, breast cancer, and papillary thyroid carcinoma [ 12 – 14 ]. However, to date, the function of HSDL2 in melanoma remains unclear.…”

Section: Introductionmentioning

confidence: 99%

Cucurbitacin E inhibits cellular proliferation and induces apoptosis in melanoma by suppressing HSDL2 expression

et al. 2022

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Background Melanoma is among the most aggressive types of skin malignancy and can have an unpredictable clinical course. Exploration of novel therapeutic targets and their regulators remains essential for the prevention and treatment of melanoma. Methods HSDL2 protein levels were examined by immunohistochemistry. The roles of HSDL2 in cell proliferation and apoptosis were identified by CCK-8 and colony formation assays. The function of HSDL2 in cell apoptosis was analysed by flow cytometry. Western blotting, cell proliferation and apoptosis and a xenograft tumour model were utilized to explore the inhibitory functions and mechanisms of CuE in melanoma. Results HSDL2 is overexpressed in melanoma and promotes melanoma progression by activating the ERK and AKT pathways. CuE could inhibit the ERK and AKT pathways by decreasing HSDL2 expression; therefore, CuE could inhibit melanoma growth in vitro and in vivo. Conclusion HSDL2 may be a promising therapeutic target against melanoma, and CuE can inhibit melanoma by downregulating HSDL2 expression.

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HSDL2 Acts as a Promoter in Pancreatic Cancer by Regulating Cell Proliferation and Lipid Metabolism

Cited by 9 publications

References 31 publications

Effects of High-Fat Diet on Cardiovascular Protein Expression in Mice Based on Proteomics

Effects of High-Fat Diet on Cardiovascular Protein Expression in Mice Based on Proteomics

MiR-26a-5p regulates proliferation, apoptosis, migration and invasion via inhibiting hydroxysteroid dehydrogenase like-2 in cervical cancer cell

Cucurbitacin E inhibits cellular proliferation and induces apoptosis in melanoma by suppressing HSDL2 expression

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