Hengning Ke's research while affiliated with Duke University and other places

... A shift from the autophagic flux response to necroptotic cell death has been observed when nitrogen-doped titanium dioxide (N-TiO 2 ) nanoparticles were photoactivated in melanoma cells [88]. Several investigations have reported that the potential to trigger necroptosis in melanoma might be inhibited due to low expression levels of both CYLD [89] and RIPK3 in melanoma cell lines [90,91]. ...

... Interestingly, recent investigations have revealed that JunB influences the infiltration of macrophages and neutrophils within the TME; however, its ultimate effect is paradoxical, suggesting a dual role of JunB in tumorigenesis and development (Arakaki et al., 2016;Wutschka et al., 2021), possibly through regulation of immune cell differentiation and effector functions. While JunB acts as a tumor suppressor in leukemia (Passegue et al., 2001), breast cancer (Wutschka et al., 2021), prostate cancer (Konishi et al., 2008), and epidermal neoplasia (Jin et al., 2011), it behaves as an oncogene in renal cancer (Kanno et al., 2012), ovarian cancer , multiple myeloma (Fan et al., 2021), and lung cancer (Suphakhong et al., 2022).To date, our understanding of relationship between JunB's immunomodulatory effects and tumor progression remains limited. ...

... Jasplakinolide has been shown to modulate (induce or arrest) various signaling pathways mediated by actin dynamics. Several studies have demonstrated that Jasplakinolide mediated actin stabilization significantly impaired growth and migration of various types of cancer cell lines including myeloid leukemia, breast, lung and prostrate carcinoma [20][21][22][23][24][25][26][27]. Consequently, given the role of jasplakinolide in modulating cytoskeletal dynamics, we were intrigued to look for its effects on SNTA1 expression/ phosphorylation and SNTA1 mediated cellular events like cell proliferation and cell migration in breast cancer cells. ...

... Aside from OmoMYC, MYC/MAX destabilizers, such as IIA6B17, 10058-F4, and 10,074-G5, and their derivatives, 3jc48-3, JY-3-094, and 3JC-91-2, can also inhibit MYC/MAX complex formation [401][402][403]. IIA6B17 has the same leucine zipper structure as c-Jun (another tumorigenesis hallmark) and can exert anti-c-Jun activity [404,405], and hence has poor selectivity and specificity as a MYC inhibitor [404,405]. JY-3-094 and 3JC48-3 inhibit MYC/MAX dimerization in cells overexpressing MYC and reduce their proliferation [406,407]. ...

... Stromal BCL2 levels are elevated in endometriosis [21,22] and GWAS-identified sequence variants of BCL2 are associated with endometriosis [18]. While BCL2 is known to inhibit cell adhesion [23], up-regulation of BCL2 has been reported in endometrial tissues [24]. Considering the increased cell adhesion activity in endometriosis, the role of BCL2 in the cell adhesion mechanism in endometriosis should be clarified. ...

... However, the connection between Cd and MAPK signaling pathway is not entirely clear. The JNK is inhibited to undergo malignant Cd transformation, to overexpress Bcl-2, and to give cells anti-apoptotic characteristics in the prostate epithelial cells [131]. It is hypothesized that the Bcl-2 overexpression could interfere with the JNK phosphorylation. ...