HCT116 colorectal liver metastases exacerbate muscle wasting in a mouse model for the study of colorectal cancer cachexia
Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured. Animal models for the study of CRC-induced cachexia, in particular mo...
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| Vydané v: | Disease models & mechanisms Ročník 13; číslo 1 |
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The Company of Biologists Ltd
01.01.2020
The Company of Biologists |
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| Abstract | Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured. Animal models for the study of CRC-induced cachexia, in particular models containing LM, are sparse; therefore, we aimed to characterize two new models of CRC cachexia. Male NSG mice were injected subcutaneously (HCT116) or intrasplenically (mHCT116) with human HCT116 CRC tumor cells to disseminate LM, whereas experimental controls received saline (n=5-8/group). Tumor growth was accompanied by loss of skeletal muscle mass (HCT116: −20%; mHCT116: −31%; quadriceps muscle) and strength (HCT116: −20%; mHCT116: −27%), with worsened loss of skeletal muscle mass in mHCT116 compared with HCT116 (gastrocnemius: −19%; tibialis anterior: −22%; quadriceps: −21%). Molecular analyses revealed elevated protein ubiquitination in HCT116, whereas mHCT116 also displayed elevated Murf1 and atrogin-1 expression, along with reduced mitochondrial proteins PGC1α, OPA1, mitofusin 2 and cytochrome C. Further, elevated IL6 levels were found in the blood of mHCT116 hosts, which was associated with higher phosphorylation of STAT3 in skeletal muscle. To clarify whether STAT3 was a main player in muscle wasting in this model, HCT116 cells were co-cultured with C2C12 myotubes. Marked myotube atrophy (–53%) was observed, along with elevated phospho-STAT3 levels (+149%). Conversely, inhibition of STAT3 signaling by means of a JAK/STAT3 inhibitor was sufficient to rescue myotube atrophy induced by HCT116 cells (+55%). Overall, our results indicate that the formation of LM exacerbates cachectic phenotype and associated skeletal muscle molecular alterations in HCT116 tumor hosts. |
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| AbstractList | Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured. Animal models for the study of CRC-induced cachexia, in particular models containing LM, are sparse; therefore, we aimed to characterize two new models of CRC cachexia. Male NSG mice were injected subcutaneously (HCT116) or intrasplenically (mHCT116) with human HCT116 CRC tumor cells to disseminate LM, whereas experimental controls received saline (n=5-8/group). Tumor growth was accompanied by loss of skeletal muscle mass (HCT116: −20%; mHCT116: −31%; quadriceps muscle) and strength (HCT116: −20%; mHCT116: −27%), with worsened loss of skeletal muscle mass in mHCT116 compared with HCT116 (gastrocnemius: −19%; tibialis anterior: −22%; quadriceps: −21%). Molecular analyses revealed elevated protein ubiquitination in HCT116, whereas mHCT116 also displayed elevated Murf1 and atrogin-1 expression, along with reduced mitochondrial proteins PGC1α, OPA1, mitofusin 2 and cytochrome C. Further, elevated IL6 levels were found in the blood of mHCT116 hosts, which was associated with higher phosphorylation of STAT3 in skeletal muscle. To clarify whether STAT3 was a main player in muscle wasting in this model, HCT116 cells were co-cultured with C2C12 myotubes. Marked myotube atrophy (–53%) was observed, along with elevated phospho-STAT3 levels (+149%). Conversely, inhibition of STAT3 signaling by means of a JAK/STAT3 inhibitor was sufficient to rescue myotube atrophy induced by HCT116 cells (+55%). Overall, our results indicate that the formation of LM exacerbates cachectic phenotype and associated skeletal muscle molecular alterations in HCT116 tumor hosts. Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured. Animal models for the study of CRC-induced cachexia, in particular models containing LM, are sparse; therefore, we aimed to characterize two new models of CRC cachexia. Male NSG mice were injected subcutaneously (HCT116) or intrasplenically (mHCT116) with human HCT116 CRC tumor cells to disseminate LM, whereas experimental controls received saline ( =5-8/group). Tumor growth was accompanied by loss of skeletal muscle mass (HCT116: -20%; mHCT116: -31%; quadriceps muscle) and strength (HCT116: -20%; mHCT116: -27%), with worsened loss of skeletal muscle mass in mHCT116 compared with HCT116 (gastrocnemius: -19%; tibialis anterior: -22%; quadriceps: -21%). Molecular analyses revealed elevated protein ubiquitination in HCT116, whereas mHCT116 also displayed elevated Murf1 and atrogin-1 expression, along with reduced mitochondrial proteins PGC1α, OPA1, mitofusin 2 and cytochrome C. Further, elevated IL6 levels were found in the blood of mHCT116 hosts, which was associated with higher phosphorylation of STAT3 in skeletal muscle. To clarify whether STAT3 was a main player in muscle wasting in this model, HCT116 cells were co-cultured with C2C12 myotubes. Marked myotube atrophy (-53%) was observed, along with elevated phospho-STAT3 levels (+149%). Conversely, inhibition of STAT3 signaling by means of a JAK/STAT3 inhibitor was sufficient to rescue myotube atrophy induced by HCT116 cells (+55%). Overall, our results indicate that the formation of LM exacerbates cachectic phenotype and associated skeletal muscle molecular alterations in HCT116 tumor hosts. Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured. Animal models for the study of CRC-induced cachexia, in particular models containing LM, are sparse; therefore, we aimed to characterize two new models of CRC cachexia. Male NSG mice were injected subcutaneously (HCT116) or intrasplenically (mHCT116) with human HCT116 CRC tumor cells to disseminate LM, whereas experimental controls received saline (n=5-8/group). Tumor growth was accompanied by loss of skeletal muscle mass (HCT116: -20%; mHCT116: -31%; quadriceps muscle) and strength (HCT116: -20%; mHCT116: -27%), with worsened loss of skeletal muscle mass in mHCT116 compared with HCT116 (gastrocnemius: -19%; tibialis anterior: -22%; quadriceps: -21%). Molecular analyses revealed elevated protein ubiquitination in HCT116, whereas mHCT116 also displayed elevated Murf1 and atrogin-1 expression, along with reduced mitochondrial proteins PGC1α, OPA1, mitofusin 2 and cytochrome C. Further, elevated IL6 levels were found in the blood of mHCT116 hosts, which was associated with higher phosphorylation of STAT3 in skeletal muscle. To clarify whether STAT3 was a main player in muscle wasting in this model, HCT116 cells were co-cultured with C2C12 myotubes. Marked myotube atrophy (-53%) was observed, along with elevated phospho-STAT3 levels (+149%). Conversely, inhibition of STAT3 signaling by means of a JAK/STAT3 inhibitor was sufficient to rescue myotube atrophy induced by HCT116 cells (+55%). Overall, our results indicate that the formation of LM exacerbates cachectic phenotype and associated skeletal muscle molecular alterations in HCT116 tumor hosts.Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured. Animal models for the study of CRC-induced cachexia, in particular models containing LM, are sparse; therefore, we aimed to characterize two new models of CRC cachexia. Male NSG mice were injected subcutaneously (HCT116) or intrasplenically (mHCT116) with human HCT116 CRC tumor cells to disseminate LM, whereas experimental controls received saline (n=5-8/group). Tumor growth was accompanied by loss of skeletal muscle mass (HCT116: -20%; mHCT116: -31%; quadriceps muscle) and strength (HCT116: -20%; mHCT116: -27%), with worsened loss of skeletal muscle mass in mHCT116 compared with HCT116 (gastrocnemius: -19%; tibialis anterior: -22%; quadriceps: -21%). Molecular analyses revealed elevated protein ubiquitination in HCT116, whereas mHCT116 also displayed elevated Murf1 and atrogin-1 expression, along with reduced mitochondrial proteins PGC1α, OPA1, mitofusin 2 and cytochrome C. Further, elevated IL6 levels were found in the blood of mHCT116 hosts, which was associated with higher phosphorylation of STAT3 in skeletal muscle. To clarify whether STAT3 was a main player in muscle wasting in this model, HCT116 cells were co-cultured with C2C12 myotubes. Marked myotube atrophy (-53%) was observed, along with elevated phospho-STAT3 levels (+149%). Conversely, inhibition of STAT3 signaling by means of a JAK/STAT3 inhibitor was sufficient to rescue myotube atrophy induced by HCT116 cells (+55%). Overall, our results indicate that the formation of LM exacerbates cachectic phenotype and associated skeletal muscle molecular alterations in HCT116 tumor hosts. Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle (SkM) wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied, and uncured. Animal models for the study of CRC-induced cachexia, in particular models containing LM are sparse, thus we aimed to characterize two new models of CRC cachexia. Male NSG mice were injected subcutaneously (HCT116) or intrasplenically with human HCT116 CRC tumor cells to disseminate LM (mHCT116), while experimental controls received saline (n= 5-8/group). Tumor growth was accompanied by loss of SkM mass (HCT116: -20%; mHCT116: -31%; quadriceps muscle) and strength (HCT116: -20%; mHCT116: -27%), with worsened loss of SkM mass in mHCT116 compared to HCT116 (gastrocnemius: -19%; tibialis anterior: -22%; quadriceps: -21%). Molecular analyses revealed elevated protein ubiquitination in HCT116, whereas mHCT116 also displayed elevated Murf-1 and Atrogin-1 expression, along with reduced mitochondrial proteins PGC1α, OPA1, Mitofusin-2, and Cytochrome-C. Further, elevated IL-6 levels were found in the blood of mHCT116 hosts, which was associated with higher phosphorylation of STAT3 in SkM. To clarify if STAT3 was a main player in muscle wasting in this model, HCT116 cells were co-cultured with C2C12 myotubes. Marked myotube atrophy (-53%) was observed, along with elevated phospho-STAT3 levels (+149%). Conversely, inhibition of STAT3 signaling by means of a JAK/STAT3 inhibitor was sufficient to rescue myotube atrophy induced by HCT116 cells (+55%). Overall, our results indicate that the formation of LM exacerbates cachectic phenotype and associated SkM molecular alterations in HCT116 tumor hosts. Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority of CRC patients, cachexia remains underserved, understudied and uncured. Animal models for the study of CRC-induced cachexia, in particular models containing LM, are sparse; therefore, we aimed to characterize two new models of CRC cachexia. Male NSG mice were injected subcutaneously (HCT116) or intrasplenically (mHCT116) with human HCT116 CRC tumor cells to disseminate LM, whereas experimental controls received saline (n=5-8/group). Tumor growth was accompanied by loss of skeletal muscle mass (HCT116: −20%; mHCT116: −31%; quadriceps muscle) and strength (HCT116: −20%; mHCT116: −27%), with worsened loss of skeletal muscle mass in mHCT116 compared with HCT116 (gastrocnemius: −19%; tibialis anterior: −22%; quadriceps: −21%). Molecular analyses revealed elevated protein ubiquitination in HCT116, whereas mHCT116 also displayed elevated Murf1 and atrogin-1 expression, along with reduced mitochondrial proteins PGC1α, OPA1, mitofusin 2 and cytochrome C. Further, elevated IL6 levels were found in the blood of mHCT116 hosts, which was associated with higher phosphorylation of STAT3 in skeletal muscle. To clarify whether STAT3 was a main player in muscle wasting in this model, HCT116 cells were co-cultured with C2C12 myotubes. Marked myotube atrophy (–53%) was observed, along with elevated phospho-STAT3 levels (+149%). Conversely, inhibition of STAT3 signaling by means of a JAK/STAT3 inhibitor was sufficient to rescue myotube atrophy induced by HCT116 cells (+55%). Overall, our results indicate that the formation of LM exacerbates cachectic phenotype and associated skeletal muscle molecular alterations in HCT116 tumor hosts. Summary: Colorectal cancer-derived liver metastases exacerbate cachexia, in line with activation of STAT3 signaling. STAT3 inhibition may improve cancer-associated muscle wasting. |
| Author | Bonetto, Andrea Pin, Fabrizio Huot, Joshua R. Novinger, Leah J. |
| AuthorAffiliation | 1 Department of Surgery , Indiana University School of Medicine , Indianapolis, IN 46202 , USA 2 Department of Otolaryngology – Head & Neck Surgery , Indiana University School of Medicine , Indianapolis, IN 46202 , USA 6 Simon Cancer Center, Indiana University School of Medicine , Indianapolis, IN 46202 , USA 3 Department of Anatomy, Cell Biology and Physiology , Indiana University School of Medicine , Indianapolis, IN 46202 , USA 4 Indiana Center for Musculoskeletal Health, Indiana University School of Medicine , Indianapolis, IN 46202 , USA 5 IUPUI Center for Cachexia Research Innovation and Therapy, Indiana University School of Medicine , Indianapolis, IN 46202 , USA |
| AuthorAffiliation_xml | – name: 3 Department of Anatomy, Cell Biology and Physiology , Indiana University School of Medicine , Indianapolis, IN 46202 , USA – name: 6 Simon Cancer Center, Indiana University School of Medicine , Indianapolis, IN 46202 , USA – name: 1 Department of Surgery , Indiana University School of Medicine , Indianapolis, IN 46202 , USA – name: 4 Indiana Center for Musculoskeletal Health, Indiana University School of Medicine , Indianapolis, IN 46202 , USA – name: 2 Department of Otolaryngology – Head & Neck Surgery , Indiana University School of Medicine , Indianapolis, IN 46202 , USA – name: 5 IUPUI Center for Cachexia Research Innovation and Therapy, Indiana University School of Medicine , Indianapolis, IN 46202 , USA |
| Author_xml | – sequence: 1 givenname: Joshua R. surname: Huot fullname: Huot, Joshua R. – sequence: 2 givenname: Leah J. surname: Novinger fullname: Novinger, Leah J. – sequence: 3 givenname: Fabrizio surname: Pin fullname: Pin, Fabrizio – sequence: 4 givenname: Andrea orcidid: 0000-0002-3235-1871 surname: Bonetto fullname: Bonetto, Andrea |
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| Keywords | HCT116 Liver metastases Cachexia Skeletal muscle Colorectal cancer STAT3 |
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| Snippet | Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle wasting, i.e. cachexia. Despite affecting the majority... Colorectal cancer (CRC) is often accompanied by formation of liver metastases (LM) and skeletal muscle (SkM) wasting, i.e. cachexia. Despite affecting the... |
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| SubjectTerms | Animals cachexia Cachexia - etiology Colorectal cancer Colorectal Neoplasms - complications Colorectal Neoplasms - pathology Cytokines - blood Disease Models, Animal hct116 HCT116 Cells Humans Interleukin-6 - physiology Liver liver metastases Liver Neoplasms - secondary Male Metastasis Mice Mitochondria, Muscle - metabolism Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Musculoskeletal system skeletal muscle stat3 STAT3 Transcription Factor - antagonists & inhibitors STAT3 Transcription Factor - physiology Tumors Wasting Syndrome - etiology |
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| Title | HCT116 colorectal liver metastases exacerbate muscle wasting in a mouse model for the study of colorectal cancer cachexia |
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