TNF-α Increases IP-10 Expression in MCF-7 Breast Cancer Cells via Activation of the JNK/c-Jun Pathways

Kochumon, Shihab; Al-Sayyar, Amnah; Jacob, Texy; Hasan, Amal; Al-Mulla, Fahd; Sindhu, Sardar; Ahmad, Rasheed

doi:10.3390/biom11091355

Cited by 10 publications

(3 citation statements)

References 63 publications

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“…Evidence has revealed a pro-tumorigenic role of TNF-α during BC progression and metastasis [83]. Kochumon et al (2021) showed that TNF-α activates the c-Jun NH 2 -terminal kinase (JNK/c-Jun) signaling pathway [84], promoting stem cell phenotype and tumorigenesis in TNBC through upregulation of the Notch1 signaling pathway [85], involved in normal mammary gland development as well as in BC tumorigenesis and progression [86].…”

Section: Bc Immune Landscape and Bc Disparitiesmentioning

confidence: 99%

Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era

Neagu,

Bruno,

Johnson

et al. 2024

IJMS

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Precision oncology is based on deep knowledge of the molecular profile of tumors, allowing for more accurate and personalized therapy for specific groups of patients who are different in disease susceptibility as well as treatment response. Thus, onco-breastomics is able to discover novel biomarkers that have been found to have racial and ethnic differences, among other types of disparities such as chronological or biological age-, sex/gender- or environmental-related ones. Usually, evidence suggests that breast cancer (BC) disparities are due to ethnicity, aging rate, socioeconomic position, environmental or chemical exposures, psycho-social stressors, comorbidities, Western lifestyle, poverty and rurality, or organizational and health care system factors or access. The aim of this review was to deepen the understanding of BC-related disparities, mainly from a biomedical perspective, which includes genomic-based differences, disparities in breast tumor biology and developmental biology, differences in breast tumors’ immune and metabolic landscapes, ecological factors involved in these disparities as well as microbiomics- and metagenomics-based disparities in BC. We can conclude that onco-breastomics, in principle, based on genomics, proteomics, epigenomics, hormonomics, metabolomics and exposomics data, is able to characterize the multiple biological processes and molecular pathways involved in BC disparities, clarifying the differences in incidence, mortality and treatment response for different groups of BC patients.

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Section: Bc Immune Landscape and Bc Disparitiesmentioning

confidence: 99%

Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era

Neagu,

Bruno,

Johnson

et al. 2024

IJMS

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“…Total cellular RNA was extracted using the RNeasy Mini Kit (Qiagen, Valencia, CA, USA), following the manufacturer's instructions. Complementary DNA (cDNA) was synthesized using 1 µg of total RNA following the guidelines from the high-capacity cDNA reverse transcription kit (Applied Biosystems, Foster City, CA, USA) [22][23][24][25][26][27]. For each real-time PCR reaction, 50 ng of cDNA template was amplified using Inventoried TaqMan Gene Expression Assay products (mouse IL-6: Hs00446190_m1; 1) Pparg: Mm00440940_m1;Fabp4: Mm00445878_m1; mouse GAPDH:Mm99999915_g; human IL-6: Hs00985639_m1; Ppar g: Hs01115513_m1; PLIN2: Hs00605340_m1; 1; human GAPDH: 4310884E using two gene-specific primers, one TaqMan MGB probe (6-FAM dye-labeled), a TaqMan ® Gene Expression Master Mix (Applied Biosystems, Foster City, CA, USA), and a 7500 Fast Real-Time PCR System (Applied Biosystems, Foster City, CA, USA) [28][29][30][31].…”

Section: Real-time Rt-pcrmentioning

confidence: 99%

IL-1β and TNFα Cooperativity in Regulating IL-6 Expression in Adipocytes Depends on CREB Binding and H3K14 Acetylation

Al-Roub

Madhoun

Akhter

et al. 2021

Cells

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IL-6 was found to be overexpressed in the adipose tissue of obese individuals, which may cause insulin resistance. However, the regulation of IL-6 in adipocytes in obesity setting remains to be explored. Since IL-1β and TNFα are increased in obese adipose tissue and promote inflammation, we investigated whether cooperation between IL-1β and TNFα influences the production of IL-6. Our data show that IL-1β and TNFα cooperatively enhance IL-6 expression in 3T3L-1 adipocytes. Similar results were seen in human adipocytes isolated from subcutaneous and visceral fat. Although adipocytes isolated from lean and obese adipose tissues showed similar responses for production of IL-6 when incubated with IL-1β/TNFα, secretion of IL-6 was higher in adipocytes from obese tissue. TNFα treatment enhanced CREB binding at CRE locus, which was further enhanced with IL-1β, and was associated with elevated histone acetylation at CRE locus. On the other hand, IL-1β treatments mediated C/EBPβ binding to NF-IL-6 consensus, but not sufficiently to mediate significant histone acetylation. Interestingly, treatment with both stimulatory factors amplifies CREB binding and H3K14 acetylation. Furthermore, histone acetylation inhibition by anacardic acid or curcumin reduces IL-6 production. Notably, inhibition of histone deacetylase (HDAC) activity by trichostatin A (TSA) resulted in the further elevation of IL-6 expression in response to combined treatment of adipocytes with IL-1β and TNFα. In conclusion, our results show that there is an additive interaction between IL-1β and TNFα that depends on CREB binding and H3K14 acetylation, and leads to the elevation of IL-6 expression in adipocytes, providing interesting pathophysiological connection among IL-1β, TNFα, and IL-6 in settings such as obesity.

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“…46 Chronic vaginal inflammation and changes in the immune response are related to carcinogenesis. [46][47][48] Elevated IP-10 levels are associated with cancer, 49 including breast cancer, 50 pancreatic cancer, 51 colon cancer, 52 and gastric cancer. 53 Interestingly, IP-10 may be a pathogenic factor in some diseases and may also play a role in tissue repair.…”

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confidence: 99%

Imbalance of Vaginal Microbiota and Immunity: Two Main Accomplices of Cervical Cancer in Chinese Women

Li¹,

Wu²,

Wu³

et al. 2023

IJWH

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Objective To explore the correlation of female vaginal microbiota and immune factors with cervical cancer. Methods The distribution pattern difference of vaginal microbiota of four groups of women (cervical cancer, HPV-positive CIN, HPV-positive non-CIN, and HPV-negative groups) were compared by microbial 16S rDNA sequencing. The protein chip was used to detect the composition and changes of the immune factors in the four groups. Results Alpha diversity analysis demonstrated that the diversity of the vaginal microbiota was increased as the disease develops. Among those bacteria abundant in the vaginal microbiota, Lactobacillus, Prevotella , and Gardnerella dominate at the genus level of vaginal flora. Compared with the HPV-negative group, the differentially dominant bacteria, such as Prevotella, Ralstonia, Gardnerella and Sneathia , are enriched in the cervical cancer group. Likewise, Gardnerella, Prevotella , and Sneathia are more in the HPV-positive CIN group, while Gardnerella and Prevotella in the HPV-positive non-CIN group, respectively. In contrast, Lactobacillus and Atopobium are dominant in the HPV-negative group (LDA>4log10). The concentration of inflammatory immune factors IP-10 and VEGF-A were increased in the cervical cancer group ( P < 0.05), compared with other groups. Conclusion The occurrence of cervical cancer is related to an increase of vaginal microbiota diversity and up-regulation of inflammatory immune factor proteins. The abundance of Lactobacillus was decreased while the one of Prevotella and Gardnerella were increased in the cervical cancer group, compared with other three groups. Moreover, the IP-10 and VEGF-A were also increased in the cervical cancer group. Thus, evaluation of changes in the vaginal microbiota and these two immune factor levels might be a potential non-invasive and simple method to predict cervical cancer. Furthermore, it is significant to adjust and restore the balance of vaginal microbiota and maintain normal immune function in preventing and treating cervical cancer.

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TNF-α Increases IP-10 Expression in MCF-7 Breast Cancer Cells via Activation of the JNK/c-Jun Pathways

Cited by 10 publications

References 63 publications

Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era

Biological Basis of Breast Cancer-Related Disparities in Precision Oncology Era

IL-1β and TNFα Cooperativity in Regulating IL-6 Expression in Adipocytes Depends on CREB Binding and H3K14 Acetylation

Imbalance of Vaginal Microbiota and Immunity: Two Main Accomplices of Cervical Cancer in Chinese Women

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