Yang Jin

• Xiao, Weihua; Chen, Qiong; Liu, Chunjiao; Yu, Yueer; Liu, Tianliang & Yang, Jin [Show all 9 contributors for this article] (2025). Gut microbiota in cancer: From molecular mechanisms to precision medicine applications. iMeta. ISSN 2770-5986. 4(2). doi: 10.1002/imt2.70017. Full text in Research Archive
• Deng, Ke; Pällmann, Nora; Livgård, Marte; Kildal, Wanja; Pradhan, Manohar & Fazli, Ladan [Show all 10 contributors for this article] (2025). Endoplasmic reticulum stress-driven nucleotide catabolism fuels prostate cancer. Cancer Letters. ISSN 0304-3835. 630. doi: 10.1016/j.canlet.2025.217888. Full text in Research Archive Show summary

  Endoplasmic reticulum (ER) stress is a critical regulator of cancer cell metabolism and survival. In this study, we elucidate the coordinated roles of two key ER stress mediators, Activating Transcription Factor 4 (ATF4) and X-box Binding Protein 1 spliced (XBP1s), in regulating purine homeostasis in prostate cancer (PCa) cells. We demonstrate that ATF4 directly upregulates Molybdenum Cofactor Sulfurase (MOCOS), a key enzyme in purine catabolism, while XBP1s induces the expression of xanthine dehydrogenase (XDH), the principal MOCOS target in this pathway. Knockdown of MOCOS significantly impairs PCa cell proliferation as well as prostatosphere and colony formation in vitro, and inhibits tumor growth in preclinical mouse models of PCa. Mechanistically, MOCOS suppression leads to purine accumulation, disrupts pyrimidine synthesis, and causes nucleotide imbalance, resulting in replication fork stalling. This imbalance is also accompanied by a compromised glutathione-mediated antioxidant response, rendering the cells more susceptible to DNA damage. Importantly, targeting XDH, either genetically or biochemically, also significantly hinders PCa cell growth. Collectively, our data highlight the pivotal role of ER stress-mediated purine homeostasis in sustaining PCa cell growth.

• Zhang, Tingting; Zhao, Faming; Lin, Yahang; Liu, Mingsheng; Zhou, Hongqing & Cui, Fengzhen [Show all 9 contributors for this article] (2024). Integrated analysis of single-cell and bulk transcriptomics develops a robust neuroendocrine cell-intrinsic signature to predict prostate cancer progression. Theranostics. 14(3), p. 1065–1080. doi: 10.7150/thno.92336. Full text in Research Archive
• Wang, Yong; Tao, Ruo-Lin; Yu, Dong-Sheng; Wu, Kai-Wen; Bai, Yang & Yang, Dong-Jing [Show all 11 contributors for this article] (2024). Air-ventilated normothermic mechanical perfusion improves susceptibility to donation after circulatory death and cold preservation-induced cholestatic liver injury through PPAR-γ/UGT1A1 axis. The FASEB Journal. ISSN 0892-6638. 38(16). doi: 10.1096/fj.202400773R. Full text in Research Archive
• Zhang, Tingting; Zhao, Faming; Hu, Yanxia; Wei, Jinlan; Cui, Fengzhen & Lin, Yahang [Show all 8 contributors for this article] (2024). Environmental monobutyl phthalate exposure promotes liver cancer via reprogrammed cholesterol metabolism and activation of the IRE1α-XBP1s pathway. Oncogene. ISSN 0950-9232. 43, p. 2355–2370. doi: 10.1038/s41388-024-03086-1. Full text in Research Archive
• Ünal, Bilal; Kuzu, Omer; Yang, Jin; Osorio, Daniel; Kildal, Wanja & Pradhan, Manohar [Show all 14 contributors for this article] (2024). Targeting IRE1α reprograms the tumor microenvironment and enhances anti-tumor immunity in prostate cancer. Nature Communications. 15(1), p. 1–21. doi: 10.1038/s41467-024-53039-1. Full text in Research Archive Show summary

  Unfolded protein response (UPR) is a central stress response pathway that is hijacked by tumor cells for their survival. Here, we find that IRE1α signaling, one of the canonical UPR arms, is increased in prostate cancer (PCa) patient tumors. Genetic or small molecule inhibition of IRE1α in syngeneic mouse PCa models and an orthotopic model decreases tumor growth. IRE1α ablation in cancer cells potentiates interferon responses and activates immune system related pathways in the tumor microenvironment (TME). Single-cell RNA-sequencing analysis reveals that targeting IRE1α in cancer cells reduces tumor-associated macrophage abundance. Consistently, the small molecule IRE1α inhibitor MKC8866, currently in clinical trials, reprograms the TME and enhances anti-PD-1 therapy. Our findings show that IRE1α signaling not only promotes cancer cell growth and survival but also interferes with anti-tumor immunity in the TME. Thus, targeting IRE1α can be a promising approach for improving anti-PD-1 immunotherapy in PCa.

• Jin, Yang; Kozan, Darby; Anderson, Jennifer; Hensley, Monica; Shen, Meng-Chieh & Wen, Jia [Show all 10 contributors for this article] (2023). A high-cholesterol zebrafish diet promotes hypercholesterolemia and fasting-associated liver triglycerides accumulation. BioRxiv. ISSN 0362-4331. doi: 10.1101/2023.11.01.565134. Full text in Research Archive
• Sikkeland, Jørgen; Ng, Matthew; Nenseth, Hatice Zeynep; Ünal, Bilal; Qu, Su & Jin, Yang [Show all 8 contributors for this article] (2022). STAMP2 suppresses autophagy in prostate cancer cells by modulating the integrated stress response pathway. American Journal of Cancer Research. 12(1), p. 327–336. Full text in Research Archive Show summary

  Six Transmembrane Protein of Prostate 2 (STAMP2) is critical for prostate cancer (PCa) growth. We previously showed that STAMP2 regulates the expression of stress induced transcription factor ATF4, which is implicated in starvation-induced autophagy. We therefore investigated whether STAMP2 is involved in the regulation of autophagy in PCa cells. Here we show that STAMP2 suppresses autophagy in PCa cells through modulation of the integrated stress response axis. We also find that STAMP2 regulates mitochondrial respiration. These findings suggest that STAMP2 has significant metabolic effects through mitochondrial function and autophagy, both of which support PCa growth.

• Xiao, Rourou; You, Lixin; Zhang, Li; Guo, Xichen; Guo, Ensong & Zhao, Faming [Show all 29 contributors for this article] (2022). Inhibiting the IRE1α Axis of the Unfolded Protein Response Enhances the Antitumor Effect of AZD1775 in TP53 Mutant Ovarian Cancer. Advanced Science. 9(21). doi: 10.1002/advs.202105469. Full text in Research Archive Show summary

  Targeting the G2/M checkpoint mediator WEE1 has been explored as a novel treatment strategy in ovarian cancer, but mechanisms underlying its efficacy and resistance remains to be understood. Here, it is demonstrated that the WEE1 inhibitor AZD1775 induces endoplasmic reticulum stress and activates the protein kinase RNA-like ER kinase (PERK) and inositol-required enzyme 1α (IRE1α) branches of the unfolded protein response (UPR) in TP53 mutant (mtTP53) ovarian cancer models. This is facilitated through NF-κB mediated senescence-associated secretory phenotype. Upon AZD1775 treatment, activated PERK promotes apoptotic signaling via C/EBP-homologous protein (CHOP), while IRE1α-induced splicing of XBP1 (XBP1s) maintains cell survival by repressing apoptosis. This leads to an encouraging synergistic antitumor effect of combining AZD1775 and an IRE1α inhibitor MKC8866 in multiple cell lines and preclinical models of ovarian cancers. Taken together, the data reveal an important dual role of the UPR signaling network in mtTP53 ovarian cancer models in response to AZD1775 and suggest that inhibition of the IRE1α-XBP1s pathway may enhance the efficacy of AZD1775 in the clinics.

• Jin, Yixin; Lorvik, Kristina Berg; Jin, Yang; Beck, Carole; Sike, Adam & Persiconi, Irene [Show all 10 contributors for this article] (2022). Development of STEAP1 targeting chimeric antigen receptor for adoptive cell therapy against cancer. Molecular Therapy Oncolytics. 26, p. 189–206. doi: 10.1016/j.omto.2022.06.007. Full text in Research Archive
• Pihlstrøm, Nicklas; Jin, Yang; Nenseth, Hatice Zeynep; Kuzu, Omer Faruk & Saatcioglu, Fahri (2021). Stamp2 expression mediated by cytokines attenuates their growth-limiting effects in prostate cancer cells. Cancers. 13(7). doi: 10.3390/cancers13071579. Full text in Research Archive Show summary

  Inflammatory events and dysregulated cytokine expression are implicated in prostate cancer (PCa), but the underlying molecular mechanisms are poorly understood at present. We have previously identified six transmembrane protein of the prostate 2 (STAMP2, also known as STEAP4) as an androgen-regulated gene, as well as a key regulator of PCa growth and survival. STAMP2 is also regulated by, and participates in, inflammatory signaling in other tissues and pathologies. Here, we show that the proinflammatory cytokines interleukin 6 (IL-6) and Interleukin 1 beta (IL-1β) significantly increase and strongly synergize in promoting STAMP2 expression in PCa cells. The two cytokines increase androgen-induced STAMP2 expression, but not expression of other known androgen target genes, suggesting a unique interplay of androgens and cytokines in regulating STAMP2 expression. Interestingly, STAMP2 knockdown significantly increased the ability of IL-6 and IL-1β to inhibit PCa cell growth in vitro. These results suggest that STAMP2 may represent a unique node through which inflammatory events mediate their effects on PCa growth and survival.

• Liu, Ming-Sheng; Zhao, Hui; Xu, Chen-Xiang; Xie, Ping-Bo; Wang, Wei & Yang, Ying-Yu [Show all 9 contributors for this article] (2021). Clinical significance of EPHX2 deregulation in prostate cancer. Asian Journal of Andrology (AJA). ISSN 1008-682X. 23(1), p. 109–115. doi: 10.4103/aja.aja_34_20. Full text in Research Archive
• Cui, Fengzhen; Pan, Qingfei; Wang, Siyi; Zhao, Faming; Wang, Runxin & Zhang, Tingting [Show all 19 contributors for this article] (2021). Maternal Benzophenone Exposure Impairs Hippocampus Development and Cognitive Function in Mouse Offspring. Advanced Science. 8, p. 1–16. doi: 10.1002/advs.202102686. Full text in Research Archive Show summary

  Benzophenones are widely supplemented in personal care products, but little is known about its neurodevelopmental toxicity. The previous epidemiological study discovered a negative correlation between maternal exposure to a benzophenone metabolite 4-hydroxybenzophenone (4HBP) and child's neurodevelopment, yet the causal relationship and detailed mechanism remain to be defined. Here, it is reported that prenatal, but not postnatal, exposure to environmentally relevant level of 4HBP impairs hippocampus development and causes cognitive dysfunction in offspring mice. Transcriptomic analyses reveal that 4HBP induces the endoplasmic reticulum stress-induced apoptotic signaling and inflammatory response in hippocampal neural stem cells. Mechanistically, 4HBP exposure activates protein kinase R-like ER kinase (PERK) signaling, which induces CHOP, inhibits IκB translation, and transactivates p65, thereby promoting inflammation and apoptosis on multiple levels. Importantly, genetic or pharmacological inhibition of PERK pathway significantly attenuates 4HBP-induced NFκB signaling and neurodevelopmental abnormalities in mice and in a human brain organoid model. The study uncovers the neurodevelopmental toxicity of BP and cautions its exposure during pregnancy.

• Pällmann, Nora; Ke, Deng; Livgård, Marte; Tesikova, Martina; Jin, Yixin & Frengen, Nicolai Sebastian [Show all 18 contributors for this article] (2021). Stress-mediated reprogramming of prostate cancer one-carbon cycle drives disease progression. Cancer Research. ISSN 0008-5472. 81(15), p. 4066–4078. doi: 10.1158/0008-5472.CAN-20-3956. Full text in Research Archive Show summary

  One-carbon (1C) metabolism has a key role in metabolic programming with both mitochondrial (m1C) and cytoplasmic (c1C) components. Here we show that activating transcription factor 4 (ATF4) exclusively activates gene expression involved in m1C, but not the c1C cycle in prostate cancer cells. This includes activation of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) expression, the central player in the m1C cycle. Consistent with the key role of m1C cycle in prostate cancer, MTHFD2 knockdown inhibited prostate cancer cell growth, prostatosphere formation, and growth of patient-derived xenograft organoids. In addition, therapeutic silencing of MTHFD2 by systemically administered nanoliposomal siRNA profoundly inhibited tumor growth in preclinical prostate cancer mouse models. Consistently, MTHFD2 expression is significantly increased in human prostate cancer, and a gene expression signature based on the m1C cycle has significant prognostic value. Furthermore, MTHFD2 expression is coordinately regulated by ATF4 and the oncoprotein c-MYC, which has been implicated in prostate cancer. These data suggest that the m1C cycle is essential for prostate cancer progression and may serve as a novel biomarker and therapeutic target. Significance: These findings demonstrate that the mitochondrial, but not cytoplasmic, one-carbon cycle has a key role in prostate cancer cell growth and survival and may serve as a biomarker and/or therapeutic target.

• Zhang, Tingting; Li, Ningning; Sun, Chaoyang; Jin, Yang & Sheng, Xia (2020). MYC and the unfolded protein response in cancer: synthetic lethal partners in crime? EMBO Molecular Medicine. ISSN 1757-4676. 12(5), p. 1–12. doi: 10.15252/emmm.201911845. Full text in Research Archive
• Jin, Yang & Saatcioglu, Fahri (2020). Targeting the unfolded protein response in hormone-regulated cancers. Trends in Cancer. ISSN 2405-8033. 6(2), p. 160–171. doi: 10.1016/j.trecan.2019.12.001. Full text in Research Archive
• Pällmann, Nora; Livgård, Marte; Tesikova, Martina; Nenseth, Hatice Zeynep; Akkus, Erman & Sikkeland, Jørgen [Show all 20 contributors for this article] (2019). Regulation of the unfolded protein response through ATF4 and FAM129A in prostate cancer. Oncogene. ISSN 0950-9232. 38, p. 6301–6318. doi: 10.1038/s41388-019-0879-2. Full text in Research Archive Show summary

  Cancer cells exploit many of the cellular adaptive responses to support their survival needs. One such critical pathway in eukaryotic cells is the unfolded protein response (UPR) that is important in normal physiology as well as disease states, including cancer. Since UPR can serve as a lever between survival and death, regulated control of its activity is critical for tumor formation and growth although the underlying mechanisms are poorly understood. Here we show that one of the main transcriptional effectors of UPR, activating transcription factor 4 (ATF4), is essential for prostate cancer (PCa) growth and survival. Using systemic unbiased gene expression and proteomic analyses, we identified a novel direct ATF4 target gene, family with sequence similarity 129 member A (FAM129A), which is critical in mediating ATF4 effects on prostate tumorigenesis. Interestingly, FAM129A regulated both PERK and eIF2α in a feedback loop that differentially channeled the UPR output. ATF4 and FAM129A protein expression is increased in patient PCa samples compared with benign prostate. Importantly, in vivo therapeutic silencing of ATF4-FAM129A axis profoundly inhibited tumor growth in a preclinical PCa model. These data support that one of the canonical UPR branches, through ATF4 and its target gene FAM129A, is required for PCa growth and thus may serve as a novel therapeutic target.

• Sheng, Xia; Nenseth, Hatice Zeynep; Qu, Su; Kuzu, Ömer Faruk; Frahnow, Turid & Simon, Lukas [Show all 16 contributors for this article] (2019). IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling. Nature Communications. 10:323, p. 1–12. doi: 10.1038/s41467-018-08152-3. Full text in Research Archive Show summary

  Activation of endoplasmic reticulum (ER) stress/the unfolded protein response (UPR) has been linked to cancer, but the molecular mechanisms are poorly understood and there is a paucity of reagents to translate this for cancer therapy. Here, we report that an IRE1α RNase-specific inhibitor, MKC8866, strongly inhibits prostate cancer (PCa) tumor growth as monotherapy in multiple preclinical models in mice and shows synergistic antitumor effects with current PCa drugs. Interestingly, global transcriptomic analysis reveal that IRE1α-XBP1s pathway activity is required for c-MYC signaling, one of the most highly activated oncogenic pathways in PCa. XBP1s is necessary for optimal c-MYC mRNA and protein expression, establishing, for the first time, a direct link between UPR and oncogene activation. In addition, an XBP1-specific gene expression signature is strongly associated with PCa prognosis. Our data establish IRE1α-XBP1s signaling as a central pathway in PCa and indicate that its targeting may offer novel treatment strategies.

• Shi, Jihua; Guo, Wen-Zhi; Jin, Yang; Zhang, Hua-Peng; Pang, Chun & Li, Jie [Show all 8 contributors for this article] (2019). Recognition of HER2 expression in hepatocellular carcinoma and its significance in postoperative tumor recurrence. Cancer Medicine. 8(3), p. 1269–1278. doi: 10.1002/cam4.2006. Full text in Research Archive Show summary

  Background The ERBB2 oncogene hypothesis is challenged in hepatocellular carcinoma (HCC) with the conflicting evidences of human epidermal growth factor receptor 2 (HER2) overexpression. HER2 could be a new target as a treatment option for HCC as well as tumor recurrence after surgery. HER2 in HCC biology needs further explorations. Methods Clinical and mRNA data of HCC patients were obtained from TCGA HCC cohort, GSE89377 and GSE115018. Western Blotting and immunohistochemistry were employed to test expression of HER2, E‐cadherin, and Vimentin. In HepG2, JM1, HER2‐transfected McA cells, and TGF‐β cocultured JM1 cells, HCC biology, including cell survival, proliferation, and epithelial‐to‐mesenchymal transition (EMT) phenotypes were evaluated. Results ERBB2 mRNA amplification was found in HCC datasets, and its expression was downregulated in high grade HCC with a worse overall survival. HER2 overexpression was identified in H4IIE, HepG2, JM1 cells, and 82% (14/17) HCC samples, and tumor stage was correlated with expression of HER2, E‐cadherin, and Vimentin (P < 0.05). Trastuzumab with the high concentrations suppressed proliferation of HER2‐positive hepatoma cells (P < 0.05); in the coculture model to induce EMT of JM1 cells, HER2 expression increased with downregulated E‐cadherin and upregulated Vimentin. Trastuzumab intravenous injection inhibited in vivo tumor size and metastases (P < 0.05). Signal analysis revealed that HER2 functioned through upregulation of β‐catenin and inhibition of SMAD3. Conclusion HER2 expression pattern is linked with tumor stage and overall survival; the transforming function of HER2 is found more relevant through β‐catenin and SMAD3. HER2‐targeted treatment is recommended to suppress the HER2‐mediated tumor growth during postoperative liver regeneration.

• Wang, Yu; Wang, Kai; Jin, Yang & Sheng, Xia (2019). Endoplasmic reticulum proteostasis control and gastric cancer. Cancer Letters. ISSN 0304-3835. 449, p. 263–271. doi: 10.1016/j.canlet.2019.01.034. Full text in Research Archive
• Jalili, Mahsa; Jin, Yang; Bones, Atle M.; Olsen, Yngvar; Vadstein, Olav & Østensen, Mari-Ann [Show all 10 contributors for this article] (2019). Dietary fatty acid source has little effect on the development of the immune system in the pyloric caeca of Atlantic salmon fry. Scientific Reports. 9(27), p. 1–16. doi: 10.1038/s41598-018-37266-3. Full text in Research Archive Show summary

  The quality and relative amounts of dietary lipids may affect the health and growth of cultured Atlantic salmon. So far, little is known about their effects on the performance of the fish immune system during early life stages and, in particular their importance in the transition from endogenous nutrition (yolk) in the alevin stage to exogenous nutrition in the later fry stage. We investigated the immunomodulatory effects of fish oil, vegetable oil and phospholipid-rich oil in feeds for farmed Atlantic salmon using a transcriptomic approach. The experiment allowed a fine-scale monitoring of gene expression profiles in two tissues, the pyloric caeca of the intestine and the liver, in a 94 days-long first feeding experiment. The analysis of transcriptional profiles revealed that first feeding induced a strong immunomodulation in the pyloric caeca after 48 days of feeding, lasting up to day 94 and possibly beyond. On the other hand, the differential effect of the three dietary regimes was negligible. We interpret this upregulation, undetectable in liver, as a potentiation of the immune system upon the first contact of the digestive system with exogenous feed. This process involved a complex network of gene products involved in both cellular and humoral immunity. We identified the classical pathway of the complement system, acting at the crossroads between innate and adaptive immunity, as a key process modulated in response to the switch from endogenous to exogenous nutrition.

• Xu, Cheng; Wang, Yunfei; Tu, Qiu; Zhang, Zhiye; Chen, Mengrou & Mwangi, James [Show all 10 contributors for this article] (2018). Targeting surface nucleolin induces autophagy-dependent cell death in pancreatic cancer via AMPK activation. Oncogene. ISSN 0950-9232. p. 1–13. doi: 10.1038/s41388-018-0556-x. Full text in Research Archive
• Jin, Yang; Nenseth, Hatice Zeynep & Saatcioglu, Fahri (2017). Role of PLZF as a tumor suppressor in prostate cancer. OncoTarget. 8(41), p. 71317–71324. doi: 10.18632/oncotarget.19813. Full text in Research Archive
• Cui, Xue-Yan; Tinholt, Mari; Stavik, Benedicte; Dahm, Anders Erik A; Kanse, Sandip & Jin, Yang [Show all 11 contributors for this article] (2016). Effect of hypoxia on tissue factor pathway inhibitor expression in breast cancer. Journal of Thrombosis and Haemostasis. ISSN 1538-7933. 14(2), p. 387–396. doi: 10.1111/jth.13206. Full text in Research Archive
• Sikkeland, Jørgen; Sheng, Xia; Jin, Yang & Saatcioglu, Fahri (2016). STAMPing at the crossroads of normal physiology and disease states. Molecular and Cellular Endocrinology. ISSN 0303-7207. 425, p. 26–36. doi: 10.1016/j.mce.2016.02.013. Full text in Research Archive
• Lindstad, Torstein; Qu, Su; Sikkeland, Jørgen; Jin, Yang; Kristian, Alexandr & Mælandsmo, Gunhild [Show all 8 contributors for this article] (2016). STAMP2 is required for human adipose-derived stem cell differentiation and adiposite-facilitated prostrate cancer grown in vivo. OncoTarget. 8(54), p. 91817–91827. doi: 10.18632/oncotarget.11131. Full text in Research Archive
• Sheng, Xia; Arnoldussen, Yke Jildouw; Storm, Margrethe Larsdatter; Tesikova, Martina; Nenseth, Hatice Zeynep & Zhao, Sen [Show all 15 contributors for this article] (2015). Divergent androgen regulation of unfolded protein response pathways drives prostate cancer. EMBO Molecular Medicine. ISSN 1757-4676. 7(6), p. 788–801. doi: 10.15252/emmm.201404509. Full text in Research Archive Show summary

  The unfolded protein response (UPR) is a homeostatic mechanism to maintain endoplasmic reticulum (ER) function. The UPR is activated by various physiological conditions as well as in disease states, such as cancer. As androgens regulate secretion and development of the normal prostate and drive prostate cancer (PCa) growth, they may affect UPR pathways. Here, we show that the canonical UPR pathways are directly and divergently regulated by androgens in PCa cells, through the androgen receptor (AR), which is critical for PCa survival. AR bound to gene regulatory sites and activated the IRE1α branch, but simultaneously inhibited PERK signaling. Inhibition of the IRE1α arm profoundly reduced PCa cell growth in vitro as well as tumor formation in preclinical models of PCa in vivo. Consistently, AR and UPR gene expression were correlated in human PCa, and spliced XBP‐1 expression was significantly upregulated in cancer compared with normal prostate. These data establish a genetic switch orchestrated by AR that divergently regulates the UPR pathways and suggest that targeting IRE1α signaling may have therapeutic utility in PCa.

• Jin, Yang; Ling, Wang; Qu, Su; Sheng, Xia; Kristian, Alexandr & Mælandsmo, Gunhild [Show all 20 contributors for this article] (2015). STAMP2 increases oxidative stress and is critical for prostate cancer. EMBO Molecular Medicine. ISSN 1757-4676. 7(3), p. 315–331. doi: 10.15252/emmm.201404181. Full text in Research Archive Show summary

  The six transmembrane protein of prostate 2 (STAMP2) is an androgen‐regulated gene whose mRNA expression is increased in prostate cancer (PCa). Here, we show that STAMP2 protein expression is increased in human PCa compared with benign prostate that is also correlated with tumor grade and treatment response. We also show that STAMP2 significantly increased reactive oxygen species (ROS) in PCa cells through its iron reductase activity which also depleted NADPH levels. Knockdown of STAMP2 expression in PCa cells inhibited proliferation, colony formation, and anchorage‐independent growth, and significantly increased apoptosis. Furthermore, STAMP2 effects were, at least in part, mediated by activating transcription factor 4 (ATF4), whose expression is regulated by ROS. Consistent with in vitro findings, silencing STAMP2 significantly inhibited PCa xenograft growth in mice. Finally, therapeutic silencing of STAMP2 by systemically administered nanoliposomal siRNA profoundly inhibited tumor growth in two established preclinical PCa models in mice. These data suggest that STAMP2 is required for PCa progression and thus may serve as a novel therapeutic target.

• Sikkeland, Jørgen; Jin, Yang & Saatcioglu, Fahri (2014). Methods to assess lipid accumulation in cancer cells. Methods in Enzymology. ISSN 0076-6879. 542, p. 407–423. doi: 10.1016/B978-0-12-416618-9.00021-2. Full text in Research Archive
• Jin, Yang; Qu, Su; Tesikova, Martina; Ling, Wang; Kristian, Alexandr & Mælandsmo, Gunhild [Show all 19 contributors for this article] (2013). Molecular circuit involving KLK4 integrates androgen and mTOR signaling in prostate cancer. Proceedings of the National Academy of Sciences of the United States of America (PNAS). ISSN 0027-8424. 110(28), p. E2572–E2581. doi: 10.1073/pnas.1304318110. Full text in Research Archive
• Lindstad, Torstein; Jin, Yang; Ling, Wang; Qu, Su & Saatcioglu, Fahri (2010). STAMPs at the Crossroads of Cancer and Nutrition. Nutrition and Cancer. ISSN 0163-5581. 62(7), p. 891–895. doi: 10.1080/01635581.2010.509836. Full text in Research Archive
• Ling, Wang; Jin, Yang; Arnoldussen, Yke Jildouw; Jonson, Ida; Qu, Su & Mælandsmo, Gunhild [Show all 11 contributors for this article] (2010). STAMP1 Is Both a Proliferative and an Antiapoptotic Factor in Prostate Cancer. Cancer Research. ISSN 0008-5472. 70(14), p. 5818–5828. doi: 10.1158/0008-5472.CAN-09-4697. Full text in Research Archive

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• Sheng, Xia; Nenseth, Hatice Zeynep; Qu, Su; Kuzu, Omer; Frahnow, Turid & Simon, Lukas [Show all 16 contributors for this article] (2024). Correction to: IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling (Nature Communications, (2019), 10, 1, (323), 10.1038/s41467-018-08152-3). Nature Communications. 15(1). doi: 10.1038/s41467-024-50645-x. Full text in Research Archive
• Wei, Ji-Fu; Xu, Tian-Rui; Yu, Ming-Can; Zhou, Xing-Ding; Zhao, Zuo-Tao & Jin, Yang (2015). Protein drugs related to allergic reaction. BioMed Research International. ISSN 2314-6133. 2015. doi: 10.1155/2015/614048. Full text in Research Archive

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